This week we talk about managing the intra-arrest period of cardiac arrest. My paradigm has changed dramatically over the past few years. In the past, I viewed the arrest as a period to teach my residents how to place a subclavian central line, how to intubate when the patient is moving, and how to cram as many drugs as possible into a patient in a short period of time.

Looking at how I manage an arrest today, so much has changed.

I use the ACLS ABCDABCD mnemonic, though I’ve changed some of the intent:

A
Place an Oropharyngeal Airway

B
Place the patient on the ventilator with a BVM mask.
Set the vent to VT 500, Flow 30 lpm, Rate 10, FiO2 100%. Increase the pressure limit to 80-100 cm H20.

C
Compressions, Compressions, Compressions

The most important thing these days are continuous, rhythmic, chest compressions. If you want to get perfusion to the coronaries and get a chance at shocking (the only other effective therapy for arrest), you need perfect compressions.

I use a metronome and switch out providers every 1-2 minutes. Got the idea from this article.

Here is the metronome I use.

ETCO2 can be used as a marker of how well compressions are being performed.

D

Defib. Shock early and shock often.

You can shock without having the compressor stop compressions if they are wearing gloves and you have a biphasic defib with pads. (Circulation 2008;117:2510-2514.)

A

Advanced airway = LMA, not an ET Tube
Here is my LMA video

B
Advanced Breathing

Put the patient back on the vent. If you know how, switch them to pressure control at 20 cm H20, with an insp time of 1-2 seconds

C
Advanced circulation

pop in an IO

listen to the podcast for my feelings on meds

D
Differential

I recommend the RUSH exam created by my colleagues and me.

Last, we talk about when to stop: for me ETCO2 < 10 and no heart motion = stop, if I have been trying for 10-20 minutes.

After the meningitis episode, one of the listeners, David Thomas, recommended I check out a new opthalmoscope from a UK company.

I checked out the web site and had them send me a sample for evaluation.

The optyse opthalmoscope is lens free, you focus on the fundi by moving closer to the patient. It is really a well made, compact, dead simple little product.

My experience was that it was far superior to the wall fundoscopes. The light was brighter and the visualization better. Unfortunately, it doesn’t hold a candle to the far more expensive panoptic. When I dilated the eyes, I had a perfect view with the optyse. In undilated, ED eyes, only the panoptic gave me a great view of the fundi.

Check out the optyse at Opthalmos’ website

Disclaimer: Opthalmos sent me an evaluation model at my request. After the evaluation I sent the product back to the company; I did not keep it. I was not paid or compensated for reviewing their product.

Hey folks,

I’m lecturing at ACEP in Las Vegas this year. This is one of two lectures I’m giving there. If you are going to the conference and plan on coming to my lecture, don’t listen to this lecture; I’d rather you hear the real one in person.

But if you can’t make it this year, and you have 50 minutes, take a listen and let me know what you think.

Here is the Handout

Here are the Slides

This week we discuss the resuscitation of the hemorrhagic shock patient with Dr. Richard Dutton, MD.

Rick was director of trauma anesthesia at the Shock Trauma Center when I trained there. He is an incredible teacher, clinician, and researcher.

Here are the take home points:

• Induction agent choice does not matter in these patients; what matters is DOSE! Reduce dose to 1/10 of full intubating dose.
• Blood products need to be available in the trauma bay for when these patients arrive. If you need to give crystalloid while awaiting the products, give only small amounts just to keep the patients heart beating.
• A systolic of 80 with good perfusion and normal sized vessels is very different than that same SBP in a patient who is clamped down. The former is a resuscitated state, the latter =spiral of death.
• The resuscitation fluid for trauma is equal parts PRBC and FFP.

To read more of Dr. Dutton’s thoughts, go to this article:

ITACCS Damage Control Anesthesia

photo from trauma.org

It seems the government and other specialties are trying hard to make sedation as difficult as possible in the ED. We must persevere to provide the best procedural sedation to allow maximal comfort and safety for our patients. This continues the discussion started in Part I, where we discussed etomidate, ketamine, and versed/fentanyl. In this podcast, I discuss propofol, ketofol, and dexmedetomidine.

the emcrit procedural sedation chapter has tons of references for all of this

Propofol

great propofol articles:

Ann Emerg Med 2008;52:392-398
Ann Emerg Med. 2007;50:182-187

Start with fentanyl 1-1.5 mcg/kg

Then give propofol 0.5-1 mg/kg

may need additional injections of 0.5 mg/kg

When patient is where you want them, begin the procedure

May need to give additional 20-30 mgs if the patient becomes too light

Burns on injection, you can precede with 20-40 mg of lidocaine to numb the vessels

Ketofol

read more here: (Ann Emerg Med. 2007;49:23-30)

1:1 mix of ketamine and propofol

In 20 ml syringe, place 10 ml of propofol (10 mg/ml)

And 10 ml of ketamine at a concentration of 10 mg/ml

Note: your ketamine may come in a different concentration, if so dilute down to 10 ml of 10 mg/ml

Shake like a martini

Dexmedetomidine

Precede with fentanyl 1 mcg/kg

Start with 0.5-1 mcg/kg over 10 minutes for loading dose

then use an infusion 0f 0.2-1 mcg/kg/hr

Beware in the bradycardic, hypotensive or patients with heart blocks

May need to supplement with 1-2 mg of midazolam

Procedural Sedation Checklist

here it is

Stay tuned for part III coming to you some time in the future.

This is a piece I wrote for the excellent Emergency Medicine Practice Guidelines Update, edited by my friend, Reuben Strayer.

The audio only version of Part I of the sedation talk.

It seems the government and other specialties are trying hard to make sedation as difficult as possible in the ED. We must persevere to provide the best procedural sedation for the maximal comfort and safety for our patients. This brief lecture was originally posted on the defunct EMCrit Lecture Site on 8/7/2009.

I’m reposting it here so I can post part II sometime this week.

This episode, Part I, covers general concepts on sedation as well as ketamine and etomidate/fentanyl.

Part II will cover propofol, ketofol, and dexmedetomidine.

Part III, to be done some time in the future, will cover really difficult sedations.

In a separate post, I will place an update I did for EM Practice with my fiance on sedation guidelines.

Severe CNS Infections are time dependent diagnoses! You must have a high index of suspicion, a good plan for your work-up, and rapid provision of treatment. After seeing a severely ill meningitis patient, I figured I would do a podcast on some tips and pearls on this topic.

When to Suspect

Here is the article I mentioned on establishing pretest prob:

http://pmid.us/15509818

What Antibiotics

Ceftriaxone 2g as empiric therapy in any suspected meningitis patient

If high risk or LP results are positive, also give

• Vancomycin 1 G
• Ampicillin 2g if age > 60
• Acyclovir 10  mg/kg if high RBC count, obtundation, seizures, or focal neurologic deficit
• Dexamethasone 10 mg
• Cefepime or Imipenem if hospitalized or neurosurgery patient

listen to the podcast for more and see the EMCrit chapter for more.

photo by Lapoland

An article I wrote with one of my ED Critical Care buddies, Chad Meyers, is now free on EM Practice.

Critical Care Monitoring in the ED

Chris Nickson, one of my favorite EM bloggers, wrote with some great additional resources on calcium channel blocker overdose.

I love that story about the successful use of ONE THOUSAND units of insulin in severe CCB toxicty – without any adverse effects. Indeed, the early use of high-dose insulin euglycemic therapy (HIET) for CCB overdoses is a subject close to my heart (http://lifeinthefastlane.com/2009/09/insulin-for-verapamil-overdose/).

Also, I’ve got a “case-based Q and A” that EmCrit listeners may find useful for learning/ testing their knowledge on CCB overdose and HIET here: http://lifeinthefastlane.com/2010/02/toxicology-conundrum-028/ (…where an infamous Australian pharmacist-blogger almost meets his demise).

Hope EmCrit listeners find the LitFL links useful.

Cheers,
Chris

 

 

Also, asked Leon for a review article and he recommended this one:

Calcium and Beta-Blocker OD Review

This week, I am joined by Leon Gussow, MD of the excellent blog: The Poison Review (TPR). TPR is my source for new toxicology articles; I highly recommend it as an incredible read. I got to meet Leon for a few beers a month ago; he is a great guy.

My Canadian pal, Ram, suggested calcium channel blocker OD as a podcast episode. Ram, here you go.

Calcium Channel Blocker OD

CCB Classes

Nifedipine and other dihydropyridines (amlodipine, felodipine, isradipine, nicardipine, nimodipine, nisoldipine) will cause profound hypotension without bradycardia, due to poor affinity for myocardial calcium channels.  This selectivity is not lost in overdose.  They may actually present with reflex tachycardia

How to tell CCB OD from B-Blocker

CCBs do not cause AMS

CCBs block receptor in B-Islet cells, preventing insulin release, so can see hyperglycemia as opposed to the normal-low sugar in B-Blockers

Presentation

Weak/Dizzy, mild confusion, bradycardia progressing to severe hypotension and shock

Selectivity is lost in overdose (except dihydropyridines)

Treatment

·        Activated Charcoal x 1

·        Whole bowel-Irrigation is not recommended by Leon’s group

·        Frequent glucose and k checks

·        Atropine (can try it once, but it will limit gastric motility and probably won’t work)

·        Calcium, 1 g of CaCl or 3 g of CaGluc.  Give slowly over 3 minutes for CaCl and 10 min for CaGluc.

·        Glucagon 5 mg bolus, probably won’t do much, unlike in beta blocker OD

·        IVF

·       High Dose Insulin. Start with 1 unit/kg push followed by 0.5-1 unit/kg/hr. Fingersticks q30 minutes and adequate glucose replacement if needed. Check potassium; supplement if < 2.5. (Crit Care 2006;10:212)

·        May need to use norepinephrine or dopamine (alternatively Epi). May need much higher doses of epi or norepi. Dopamine must be stopped at 20 mcg/kg/min, which is kind of a joke in this OD. Switch to one of the others if you get this high.

·        Levosimendan may have a role, but not available in the US.

·        IABP, CP Bypass

<photo by ilovespoons>

At this stage of the game, if your hospital is not offering hypothermia to out-of-hospital cardiac arrests, you are probably lagging behind optimal care. For shockable rhythms, you essentially double your patient’s chances of leaving the hospital with good neurological outcome. However hypothermia can be tough, unless you have done a bunch. Learn from my mistakes in this lecture.

Here is the link to the slideset

I’d love to hear your comments and what you are doing at your hospital.

for more hypothermia resources, see my NYC Hypothermia Site

When I was a resident, every vent lecture either put me to sleep or left me dazed and bewildered. I gave a lecture of that ilk when I started working after fellowship. I had become part of the problem. I decided there must be a way to make vent management more understandable and if not interesting, at least bearable.

This lecture was up on the soon to be defunct EMCrit Lecture site. It offers a path to managing any patient on the ventilator in the ED. I have tried to simplify as much as possible while still maintaining an evidence-based approach.

This is Part II, it deals with the obstructive strategy. Last week, we spoke about the strategy for patients with  lung injury.

Your goal with these patients is to let them have adequate time to breathe out.

There are only 4 things you need to remember for an obstructive patient

Vt (Tidal Volume) = 8 ml/kg, don’t mess with it

Flow Rate = shorter insp times, 80-100 lpm

Resp Rate = Lung protection, start at 10 work your way down if necessary

FiO2/PEEP = Oxygenation, should need much O2 (40%)m I recommend PEEP of 0, but certainly keep it less than 5

First Print out this Handout

If you need just the audio [right or cntrl click here]

Click here to view the embedded video.

Dr. Gentile responded to a few listener questions below:

HOW  DIPHENHYDRAMINE ENTERED PROTOCOL

when i first started using “high”  dose opiates for the most severe patients about one third of them experienced nausea and or vomiting. Sometimes the guy in bed 2 vomits, then after /during mop up the girl in bed 3 vomits, the woman in 5 is here for asthma she is offended by  the smell and she vomits too. i was not popular with housekeeping but i was much appreciated by those who received the opiates. i asked some of the worst vomiters if the vomiting was worse than the pain. Every single one said the vomiting was no problem ,and they felt better vomiting than they did in pain. Some even vomited while they were answering the question.

The next leap was giving IV antiemetic prophylactically, with the first dose of morphine. i initially felt some trepidation giving anti-emetic when 2/3 of patients probably would not benefit from the drug. Then i remembered demerol and phenergan had been given together for ages. i felt validated by this precedent and forged ahead.  it worked great and the vomiting/mopping cycle stopped. Housekeepers stopped giving me the stink-eye.

My favorite anti-emetic was compazine. There were a few dystonic reactions and some akisthesia but overall it was a success.

Compazine was unavailable for a few years and i switched to droperidol. The droperidol gave a lot less dystonia and less akisthesia, so that too was progress. Hundreds of happy doses of droperidol and no problems. It was a useful adjunct for analgesia,

Droperidol was great for nausea and vomiting without pain. Many of the vomiting patients reaped the benefit of central dopamine antagonism as well  [Some people with abdominal pain are crazy ]. What a great drug. Droperidol got black boxed. Once again the interests of the suffering masses were sacrificed to the interests of big pharm. The instrument of destruction was our FDA, an organization that is supposed to protect people from big pharm. I started looking for other options.

A haldol overdose came in one day and i was reading about butyrophenone overdose and discovered the butyrophenones [haldol, droperidol] have antihistamine side effects. That’s when i had the insight that histamine was the real culprit causing the the vomiting.

Histamine causes an itchy feeling when the opiate goes into the vein, histamine causes hypotension, histamine causes nausea and vomiting. Do all anti-emetic drugs have anti histamine “side-effects”.  Compazine yes reglan yes droperidol yes tigan yes phenergan yes. Zofran [i'm not sure]. I would call this more than an interesting coincidence. The antihistamine side effect of anti-emetic drugs might be the mechanism of action, not really a side -effect at all.

Have you seen an orthopedic injury that hurts so bad the patient vomits? Do endogenous opiates cause histamine release?

Many ER patients have abdominal pain and vomiting; most of the time the pain protocol gets rid of both the pain and the vomiting.  Not true with small bowel  obstructions but most of the time additional “anti-emetic” is not needed.

so diphenhydramine went into the protocol; and life is very good. i got a little sad that patients receiving state of the art acute analgesia were getting admitted to the hospital and taking the elevator to 1960. i thought it might be nice if admitted pain protocol patients got a PCA pump automatically. i started reading about PCA pump protocols and most of them use diphenhydramine and morphine. The PCA literature validates what i “discovered”. The anesthesiologist/oncologists that developed PCA have known that diphenhydramine is useful for a long time.

Diphenhydramine at .5 mg/kg does not make old or young people too sleepy. Some people on the protocol go to sleep. Some of the patients are tired. If i was awake at home for three days with a broken hip, i would go to sleep the moment someone took the edge off my pain. Some of the patients are bored to sleep. If i was in the ER gurney without a book what are my options [read "patient rights and responsibilities" again, watch my heart rhythm, or sleep.] Sleep is not a little dead. Sleep is good.

i do not have references to support my statements about hypotension. Only my subjective observations that there have been a lot less of this conversation at work since we started using diphenhydramine.

aren’t you tired of this conversation.

nurse———–”the blood pressure is down in clinic 7 bed”

doctor—–”give em 500 normal saline stat”

10 minutes later

nurse——”the pressure is back up”

doctor—-”good”

was the patient in bed 7 sick? did they get better? was their life saved or even subtly improved by a transient change in a measurement they can not feel?

i agree that a blood pressure of zero is usually bad, but if my blood pressure drops 10% i am not 10% dead. The culture around blood pressure measurements and reactions/over reactions in the E.R. is irrational.

The less time spent on this futile ritual the better. i am sure there has been less of this since diphenhydramine was included. i did not count it or study it. i just noticed it like i notice the weather is usually sunny on my way to work. It’s true. if you like sun move to southern california.

When I was a resident, every vent lecture either put me to sleep or left me dazed and bewildered. I gave a lecture of that ilk when I started working after fellowship. I had become part of the problem. I decided there must be a way to make vent management more understandable and if not interesting, at least bearable.

This lecture was up on the soon to be defunct EMCrit Lecture site. It offers a path to managing any patient on the ventilator in the ED. I have tried to simplify as much as possible while still maintaining an evidence-based approach.

This is Part I, it deals with the lung injury strategy. Next week, we’ll talk about the strategy for patients with obstructive lung disease.

There are only 4 things you need to remember for a lung injury patient:

Vt (Tidal Volume) = Lung Protection

Flow Rate = Patient Comfort

Resp Rate = Ventilation

FiO2/PEEP = Oxygenation

First Print out this Handout

If you need just the audio [right or cntrl click here]

Click here to view the embedded video.

This post is just to place the vent handout into itunes.

Even when we can’t cure a patient, we can relieve suffering. On average, we kind of stink at pain control in the ED. One physician, Dr. Ed Gentile, has created a simple path to optimal acute pain control in the ED. I heard this lecture on the EM:RAP podcast and got permission from Drs. Gentile and Herbert to repost it here. This is not a critical care topic per se, but it is applicable to the critically ill, the non-critically ill–basically any patient who is in pain in the ED.

Patient Controlled Analgesia

by Ed Gentile, MD

Need for an effective and efficient process is self evident .

Acute pain protocol for moderate/severe pain

• Administer morphine 0.1 mg/kg IVP (If pt is > 55 y/o, substitute morphine 0.05 mg/kg IVP for this 1st dose)
  + diphenhydramine 0.5 mg/kg IVP
• 7 minutes later the patient is asked, “Would you like more pain medicine?”
• If the answer is yes, give a 2nd dose of morphine 0.05 mg/kg IVP
• 7 minutes later, the patient is asked again, “Would you like more pain medicine?”
• If the answer is yes, give a 3rd dose of morphine 0.05 mg/kg IVP
• This continues every 7 minutes until the patient answers “no” to the question or the patient is asleep.

According to Dr. Gentile, “We don’t want to use the minimum, but the optimum pain dose for all patients.”

The protocol uses morphine because it has the longest half-life .

Diphenhydramine prevents antihistamine effects: nausea, vomiting, hypotension.

The protocol is unbiased and controlled by the patient!

Photo by Azarius

Rob Orman has a fantastic podcast called the ERCast. You can also search for “ercast” on itunes. He was kind enough to have me on his latest episode. Check it out if you like.

Hi folks,

I received a bunch of emails asking how to get the old episodes into itunes. I expanded the RSS feed to include them, now you just need to bring them into itunes, this 40 second video shows you how.

We’re still working on the Greater NY Sepsis Initiative. The next step towards making a non-invasive protocol possible is to teach folks how to use ultrasound of the IVC to assess fluid responsiveness. I developed this video to get ED & ICU docs up to speed. If you can do ANY ultrasound exam, you can do this one.

If you want to see the most recent version of the non-invasive protocol:

Non-Invasive Protocol

The invasive protocol that goes with it can be seen here:

Invasive Protocol

Click here to view the embedded video.

photo from wikipedia

Aggressive palliative care is just as important as aggressive critical care in the ED. Sometimes we will be the first physicians to talk to a family about end of life issues, even if their loved one is terminally ill. Now that is not how it should be, but it just means that we must be just as skilled at family palliative care discussions as we are at floating a transvenous pacer. In this podcast, I discuss my vision of how to handle palliative care issues in the ED.

Step I-Identify potential comfort care patients

Step II-Establish goals of care

Either aggressive curative or aggressive comfort. Sometimes, you will decide with the family to a “trial” of critical care

Step III-Sign the Paperwork

Step IV-Maximize comfort

start a fentanyl drip

consider glycopyrrolate or a scopolamine patch

Remember the concept of double effect

photo by P Nicholson

Two listener questions answered in 5 minutes

From Dr. Ram Reddy of Canada:

Great thought to intubate a patient in hemodynamic extremis using the awake approach. I can’t tell you how many times I’ve given etomidate only to have to yell \start CPR\ immediately after( and i just started working). So this stuff about etomidate being HD stable is bullshit, when the pressure is super low.

With Regard to awake intubation for the HD unstable patient. My worry is two fold

1) when you are looking to secure the airway of somebody with a systolic of 50, the time required to administer glyco, nebulize lido, gargle( if they can) and atomize is too lengthy

2) I’m also willing to wager that the scenario where you don’t really get great topicalization is more common then maybe we think. now you have a patient gagging, bucking, fighting, making 1st pass success more difficult. if they get complete topicalization then i guess I would look heroic, but if it’s partial, and they fight you or the muscular tone remains too high to visualize cords well, i think it could look like a gong show? then you are stuck with going back to a conventional RSI with the disadvantage of having manipulated the airway already. what do you think?

how about a modified RSI, quick bolus of fluid, 500 of phenyl + half induction dose ketamine + succs + apologize later, if they live to remember that they were paralysed with some awareness. this is the typical induction for the anaesthetists when they need to do a trauma lap on a hypotensive patient at my institution.

this question refers to Podcast 23

——

from Dr. Ram Parekh of my shop:

the copd-er had a pH 7.05 and pCO2 119 at the time I decided to intubate, despite NIV and nebs. I put him on NIV SIMV with a minimum rate of 18 (using EtCO2 as a guide) , tv 550, FiO2 100% to make sure he ventilates some while pushing the meds before intubating.

Any thoughts? How are you optimizing your hypercarbic resp failure patients?

this question refers back to Podcast 3

Darren Braude, Aiway and EMS master from New Mexico demonstrates the use of a bougie to make the cric procedure MUCH easier. For more great Braude magic, see his site at airway911.com.

Click here to view the embedded video.

This is a video by my friend Seth Manoach, MD. He has been an EM Physician for many years and now is in the midst of a three year critical care fellowship sojourn.

This video demonstrates the fiberoptic stylet-aided cric. In this case he is using a Levitan Scope, but an adult bonfils or any other rigid fiberoptic should work fine.

The airway he is using is the Melker cuffed cric catheter, but I have tried this in trach incisions with 6-0 ET tubes, and 6.0 trach tubes as well.

Here is the article seth put in the literature:

Resuscitation. 2009 Sep;80(9):1066-9.  Development of a rapid, safe, fiber-optic guided, single-incision cricothyrotomy using a large ovine model: a pilot study.

Please note: The sheep in this video was treated with the utmost respect and ethics. It was heavily sedated throughout with tons of thiopental plus ketamine and xylazine.

Click here to view the embedded video.

Download the video here

Here is my video on performing open cricothyrotomy in 3 situations: with a trach set and an assistant, with a trach set when alone, and when you only have a scalpel.

Click here to view the embedded video.

Download the video here

Ok, Ok, I promise this is the last airway episode for at least a little while. I am perhaps a bit obsessed. Had this show in the works for a while. The cric is the last barrier between a failed airway and death. EM docs need to be able to perform this procedure without hesitation. This requires training and practice until you can perform the procedure in < 30 seconds literally with your eyes closed!

On this show:

Since you need to practice and patients get a wee bit pissed if they wake up with an unnecessary, unexpected tube in their neck, you need something to train on. Pig trachs smell and are not great training IMNSHO. Instead, read this article:

Anaesthesia 2004;59:1012

Here is the picture

With this set-up, which costs nothing, you can practice as many times as necessary any time you like. You’ll see my version of the set-up in my video below.

I prefer surgical crics. I think wire-based seldinger kits fail badly when stress is involved. That is opinion. They are also entirely too slow; that is FACT.

Anaesth Anal 2010;110(4):1083 & Anaesthesia 2006;61:565

Here is a video with the three techniques I prefer for crics

Click here to go to the video post

Next we talk to my friend Seth Manoach, another of the ED Intensivist clan. He has a technique for fiberoptic-stylet guided crics.

Click here to see the video

Last, we talk to Darren Braude of airway911.com fame and author of the book Rapid Sequence Intubation & Rapid Sequence Airway. Darren has a technique for bougie-aided cric that you are going to love.

Click here to see the video

photo from wikipedia

.

A lot of NYC hospitals want a non-invasive protocol for severe sepsis treatment. This is the one we are working on. If you get a chance take a look and tell me what you think in the comments section. I personally would be going invasive on many of these patients. But when surveyed, many ED docs have made it clear that they will not be placing central lines in normotensive patients.

non-invasive sepsis protocol

–Scott

photo by zacwitnij

So after the awake intubation video went up on emrap tv, I got a flurry of emails telling me how cool the concept is, but questioning who this would actually be usable on.

To answer that question, we first must discuss who actually requires intubation. If you wait until the patient is apneic, then of course you can’t use awake intubation. The idea is to intubate before the patient stops breathing.

In Ron Walls’ airway manual and in his class, he gives the following reasons for intubation:

Crash-a patient who is dead or near dead

Can’t Protect Airway

Can’t Maintain Ventilation/Oxygenation

Expected decline in Clinical Status

Now some of these make sense and some not so much

Here are my reasons to intubate:

Crash-for me this is any apneic patient

Can’t Protect Airway-this one is good, a patient with pooling secretions or obtundation with vomiting buys plastic

Possible Loss of Airway-angioedema, anaphylaxis, neck trauma. These are good reasons to intubate and usually earlier is better and safer.

Oxygenation/Ventilation issues for me mean you intervene. But this doesn’t necessarily mean intubation, if the patient has a reversible problem, put them on Non-invasive instead of intubating. See the podcast.

So it all comes down to the last reason

Expected decline-this should be the reason for many ED intubations. If the patient has O2/CO2 issues and they will be getting worse, then consider intubation.

Supply/Demand Imbalance-Last reason, not discussed as often in the ED is severe metabolic acidosis or shock where the lungs are causing a huge metabolic demand in a patient without much supply.

So who can be intubated awake? Any patient except the crash airway can be intubated awake. If you think they are a difficult airway, temporize with NIV while you topically anesthetize and then do the patient awake while they keep breathing.

Who is a difficult airway, there are few good answers.

THe LEMON rule also coined by the Walls crew is probably as good as any:

Look at head and neck

Evaluate 3-3-2

Mallampati

Obstruction

Neck Mobility

see here for more

I also discuss a new possible indication for awake intubation

photo by pig sty ave

Warning-This is not an ED Critical Care Podcast, it is a rant. Rants will be featured periodically and irregularly; feel free to ignore and delete them.

This one was spurred by a post by Chris Nickson, aka precordialthump.

The post led me to an incredible lecture by Dr. David Schriger given at the most recent All LA Conference. You should go and listen to this lecture:

Link to Dr. Schriger’s Talk at alllaconference.com

The issue of critical thinking in EM was once dear to my heart. I even wrote a book about it, when I believed that print publishing was not a bloated and dead enterprise.

But the flash and glamor of critical care soon eclipsed my love of critical thinking. However Dr. Schriger’s excellent lecture stirred up this old romance.

In this brief rant, I discuss three additional points that occurred to me as I was listening. But remember, you will be far better served using your time to listen to his lecture than my rant.

photo by Rionda

Young patient, lactate of 5.2, pneumonia… You know what you’re supposed to do–put in the central line and start early goal directed therapy. Problem is, most people can’t see sticking a central line in a patient that does not need pressors and otherwise looks well. Yet these patient have an annoying habit of going on to decompensate and perish. Well now there may be another way. Thanks to an article just published in JAMA, we may have a path to non-invasive treatment of severe sepsis. In this EMCrit Podcast, I interview Dr. Alan E. Jones, author of the article, Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. Then I discuss how this article changes the game when it comes to caring for severe sepsis patients.

First, here is the article:

[PubMed]

Dr. Alan Jones was the lead author. He and his co-authors from the EMShockNet, designed a 300-patient randomized, controlled trial in 3 academic emergency departments. Patients were adults with essentially the same entry criteria as the original EGDT study. Both groups received the EGDT protocol except one group got continuous ScvO2 monitoring while the other group got serial lactates. Either serial normal lactates (<2 mmol/L) or a decrease in lactate of greater than or equal to 10% was considered equivalent to an ScvO2 > 70. Lactates that were rising or had cleared < 10% were considered equivalent to ScvO2 < 70. Mortality trended towards a higher rate in the ScvO2 group, but by the predetermined trial parameters, both arms were considered equivalent.

I got a chance to interview Dr. Jones and we talked about the following points:

1. Though the trial did not specifically test this strategy, the purpose of the study was to find a path to non-invasive care of severe sepsis.
2. Only 10% of the patients in either arm required blood transfusions or inotropes
3. In young patients, in certain clinical scenarios, we might move to inotropes before blood, in the Hb 7-10 range.

In addition, Dr. Jones mentioned that in an upcoming preplanned sub-analysis we’ll actually get to see if the lactate clearance values and ScvO2 correlated.

I then go on to discuss how this article allows a non-invasive path to managing the young pt with severe sepsis. Let’s say we have that young pneumonia patient with a lactate of 5.2

• First, give 2L of the crystalloid of your choice
• Make sure that the SaO2 is > 90%
• Then check the IVC non-invasively with ultrasound.
• IVC < 1.5 cm and has a > 50% collapse with deep inhalation, give more fluid.
• IVC > 1.5 cm and very little collapse, move on
• Confirm that the MAP is still >65, if not then place a central line and do standard EGDT
• Check a repeat lactate. If it cleared ? 10%, then you’re done
• If it hasn’t transfuse if Hb < 7.
• Give inotropes if Hb > 10 or signs of poor heart function on echo
• Hb 7-10, use your judgment
• Keep trending the lactate

Pushing some ativan followed by vecuronium is no longer an acceptable strategy to manage post-intubation sedation. A good analgesia and sedation package is essential if you care about your patient’s comfort and well-being. We need to move to PAIN-FIRST paradigm. Optimize analgesia and then add in sedative agents as a bonus. In this episode of the EMCrit Podcast, I expand on a previous rant to discuss the optimal way to handle routine post-intubation patients and some special scenarios you may encounter.

The Routine

Here is the Lancet Article I mentioned:

(A protocol of no sedation for critically ill patients receiving mechanical ventilation: a randomised trial)

Post-Intubation patients are in pain b/c they have a piece of rigid plastic jammed down their throats and b/c we do a lot of evil-seeming stuff to them in the ED.

Give them a bolus of fentanyl or morphine as soon as you complete the intubation (or better yet, with your RSI drugs)

Fentanyl Protocol
Morphine Protocol

Only when you have a calm, relaxed, but fully awake patient, add on a touch of sedative for hypnosis, amnesia, and anxiolysis.

Use a sedation scale like RASS.

Special Scenarios

1. Hypotensive Medical Patient-the patient’s blood pressure is never too low to get adequate pain control and sedation. Start them on a pressor and give them comfort. Fentanyl/versed is probably a good combination. Maybe in the future ketamine/versed.

2. Delerium Tremens-these patients need GABA first. My patients have already received 200-400 mg of diazepam before getting intubated so more benzos will probably not help. Use propofol/fentanyl. If propofol is not available, use versed/fentanyl/phenobarbital. Here is a DT protocol that encompasses phenobarb. Also see my DT Podcast.

3. Neurocritically Ill Patients-aka the head bleeds. This one is for Mike, a flight medic. Fentanyl/propofol is the way to go for these patients. Take them deep during the first 24 hours or so. Treat pain and sedation needs first, before add anti-hypertensives; their blood pressure may come down when you treat their pain. If you are transferring these patients, have a very low threshold to intubate, leaving them on propofol/fentanyl. WHen the receiving hospital gets the patient, they can easily extubate them if you used these medications.

Here is my extubation article.

4. Hypotensive Trauma Patients-this pertains to trauma patients hypotensive because of hemorrhagic shock.  I get a bunch of ketamine and a bunch of fentanyl. If their MAP > 65 then I give 25 mcg of fentanyl. Wait a couple of minutes and if still > 65, give some more. If their MAP < 65, I give 10-15 mg of ketamine. Keep going with this until your patient looks good.

photo by brentbat

Your patient is pale and diaphoretic. Blood pressure is 70/50. Heart rate is 178. EKG shows atrial fibrillation… What are you going to do???

Yeah, yeah the Pavlovian ACLS response–You cardiovert. Wonderful, except it didn’t change a thing. Now what?

In this episode, I discuss the crashing atrial fibrillation patient.

Shock

If the patient is chronically in atrial fib, the shock rarely works. Your patient is unstable, so you decide to give it a shot. You might as well give yourself the best chance of success, so go right for 360 J on monophasic, or equivalently high on your biphasic. This will not cause more injury than lower joules (Heart 1998, 80:3 and Resuscitation 1998;36:193). PA is probably better than AA if you have pads. Make sure the synch is on.

You need to give your patient something to disguise the fact that you are electrocuting them. Yet you don’t want to drop their pressure. Ketamine is ok in disassociative dosing, but then your patient is loopy and you lose your mental status exam. Consider 5-7 mg of etomidate along with a pain dose of ketamine, 10-15 mg.

Screen for WPW

If you have a. fib with a wide QRS and a rate > 250-300, be scared, very scared. This is WPW and these patients just love to ruin your day by going into v. fib. Shock early, shock often, light them up.

Get the BP Up

So you made sure it’s not WPW and the cardioversion has failed, as it so often does in chronic a. fib. Now you need to raise the BP before anything else. Use push-dose phenylephrine. 50-200 mcg every minute or so until you get the blood pressure above a diastolic of 60; this will temporize the situation and make the patient’s heart more likely to slow down.

Though things look better, you have not really fixed the problem, you have just temporized.

Slow them them down

Give either amiodarone 150 mg bolus and then the drip (may repeat the bolus x 1)

Or

Use diltiazem, but not as a push. Drip it in at 2.5 mg/minute until HR < 100 or you get to 50 mg. See here for more.

Still not working?

• Consider magnesium
• Consider reshocking
• Consider cardiology consult
• Consider something else is going on
• Consider signing out to one of your colleagues and running away

Intubation is a sexy procedure, there is no doubt about it.

NIV does not have the glamour; it’s not nearly as cinematic. But for the patient, to spend 30 minutes on a NIV mask is preferable to a couple of days on the ventilator. In this episode, I discuss some of the basic ideas and methods of NIV.

It is pretty simple as the mode only has 3 main settings:

FiO2 – set based on oxygen requirements, just like on the vent

PEEP/EPAP/CPAP – all the same thing, set this based on OXYGENATION needs. If the patient’s sat is low, start at 5 cm H20 and titrate up to 15-17 as needed.

PSV/IPAP – this setting is for ventilation. If your patient does not have ventilation problems, they don’t need PSV. If they do, start at 5 cm H20 and titrate to 15-17.

Yes, that’s right, I did not tell you to put every patient at 10/5. Very few of your patients will have both ventilatory and oxygenation problems. Asthma and COPD need inspiratory support. APE, atelectasis, pneumonia patients need PEEP.

I also talk about sedation while a patient is on NIV.

The Utopian College of Emergency for Medicine with the help of the lifeinthefastlane blog, has taken my Upstairs Care, Downstairs philosophy to its next logical conclusion. I can’t believe I did not see this myself.

read more here

Awake intubation can save your butt!

It requires forethought and humility–you must be able to say to yourself, “I am not sure I will be able to successfully intubate this patient.” However, the payoff for this thought process is enormous. You can attempt an intubation on a difficult airway with very few downsides. If you get it, you look like a star, if you don’t you have not made the situation worse.

Two of my critical care resident specialists, Raghu Seethala and Xun Zhong, volunteered to intubate each other awake. The purpose of this was to let them gain experience, understand what their patients would feel during the procedure, and to prove that awake intubation can be done without complicated nerve block injections or fragile equipment, such as a bronchoscope.

Here is the procedure for ED Awake Intubation–EMCrit Style:

DRY THEM OUT (Do All)

If you can give it early 10-15 min before topicalizing, it will be most effective.

• Glycopyrolate: 0.2 mg IVP (No central effects – does not cross BBB. You can use atropine, but more side effects are possible)
• Suction and then pad mouth dry with gauze – you want the mouth very dry!

TOPICALIZE (Do All)

• 5 cc of 4% lidocaine nebulized @ 5 liters per min
• Gargle with viscous lidocaine (4% best, 2% ok). Place a blob (~3 cc) on a tongue depressor, put it in the back of the throat and have the patient gargle and then spit
• Spray the epiglottis, cords, and trachea with 4% lidocaine (3 cc) in a Mucosal Atomizer Device (MAD). The patient will cough during this spraying, wear eye/face protection
• Have another syringe loaded with 4% lidocaine to spray with during the procedure

Note: the systemic and pulmonary absorption from this method is quite low. The only place to watch out is spraying the trachea. I would not spray more than 2-3 cc down the ol’ windpipe.

SEDATE (Choose one!)

• Ketamine and propofol in the same syringe makes Ketofol. The classic mix is 50 mg of ketamine to make 5 cc and 50 mg of propofol to make 5 cc. Put these both in a 10 cc syringe and shake. Depending on the patient’s hemodynamics, I sometimes will use more ketamine (75% instead of 50%). Give 1-2 cc every minute until you have the patient relaxed, but still breathing and arousable.
• Ketamine alone also works just fine. Start with 20 mg and give 10 mg every minute or so.
• If you have it, Dexmedetomidine also works very well as long as your patient is not bradycardic.
• If you have neither of these 2 mg of midazolam will do just fine.

• Preoxygenate with NRB

• Optimally position (ear to sternal notch) with the head tilted all the way back

• Restrain both arms with soft restraints to prevent the “grabbies”

• Switch to nasal cannula

• INTUBATE with Fiberoptic laryngoscope and bougie

• If the patient coughs or is uncomfortable after placing the bougie through the cords, push the remainder of the ketofol syringe.

• Thread  the tube over the bougie with the laryngoscope still in the mouth

• Confirm tube placement

That’s all for this week

For more info on awake ED intubation, you can view a complete lecture here

Thanks to Raghu and Xun for risking their singing careers and to Jimmy & Anita for technical support. *
The opinions on this site and in the video represent the author’s and not the opinions or policies of the Mount Sinai School of Medicine or Elmhurst Hospital Center. It is not my intention to provide specific medical advice for any individual patient. Please confirm anything on this video with your own clinical judgment and the policies and procedures of your institution. This video is for education purposes only; it does not represent a standard of care or clinical advice.

So you have a patient with intracranial bleeding or you have a high pre-ct suspicion of intracranial bleeding and they are taking coumadin, aspirin, or clopidogrel. Should you reverse them? If so, how?

What if the CT is negative? Can you just discharge these patients as soon as they have a negative CT?

In this episode of the EMCrit Podcast, I discuss reversal of anti-coagulant drugs & anti-platelet medications, with particular emphasis on the prothrombin complex concentrates (PCC). I also touch on how to disposition these patients if their initial CT scan is negative.

Reversal Meds

Here are sample guidelines for drug reversal:

Warfarin
Any patient with a history of recent warfarin use, with an INR > 1.5 should immediately receive:
1. Vitamin K 10 mg IVPB over 10 minutes (monitor for hypotension / anaphylaxis) &
2. 50 units/kg of Prothrombin Complex Concentrate (Bebulin or Profilnine) Administer over 20 minutes.
• If PCC unavailable, give 15 cc/kg of FFP
Repeat INR 10 minutes after completion of infusion

Liver failure with known coagulopathy or elevated PT or INR •1.5
1. Vitamin K 10 mg IV over 10 minutes (monitor for hypotension / anaphylaxis) &
2. 50 units/kg of Prothrombin Complex Concentrate (Bebulin or Profilnine) &
3. 2 units of FFP
• If PCC unavailable, give 15 cc/kg of FFP total

Reversal of Platelet Dysfunction: For any patient with antiplatelet (Aspirin, Aggrenox or Clopidogrel) used in last 24 hours administer:
1. dDAVP 0.3 mcg/kg x 1 (20 mcg in 50 cc NS over 15-30 minutes) &
2. 1 donor pack platelets (~6 units)

Review Article of Vitamin K antagonist reversal (Critical Care 2009, 13:209)

Review Article on PCCs (European Journal of Anaesthesiology 2008; 25: 784–789)

CT Negative after Head Trauma while on Anti-coagulants or Anti-plt Meds

One man’s jury-rigged approach:

Minor head trauma (the definition of this in the anticoagulant literature seems to be different than most other head trauma lit, they actually define minor as NO LOC and NO AMNESIA, just a bop to the head)

• Most folks would still say scan these patients once and then observe for 6 hours. A few would say just observe, a very few would say admit for 24 hours. I watch them for 6 hours and then get the CT scan.

Head trauma with LOC, but GCS 15

• definitely scan, definitely observe at least 6 hours, most would say either rescan or admit for 24 hours

Head trauma with LOC, but GCS < 15

• scan, almost certainly admit for 24 hours, probably rescan prior to d/c

Not great literature support for any of this, here are some studies to get you started:

Delayed Posttraumatic Acute Subdural Hematoma in Elderly Patients on Anticoagulation (Neurosurgery 58:851-856, 2006)

Low Dose ASA led to secondary bleeding not seen on initial CT in patients with normal neuro exams (J Trauma 2009 67(3):521)

Happy New Year!

Here are three of the most popular posts from 2009. Check them out if you missed them:

Sympathetic-surge Crashing Acute Pulmonary Edema – When a patient gets wheeled in with crackles up to their clavicles and a BP of 280/190, the problem is NOT volume overload. These patients need afterload reduction. And if you need to intubate them, it is on some levels a failure [Read More & Listen to the podcast]

Intubating the Critical GI-Bleeder – Nothing is as sphincter-tightening as having to tube a variceal bleed with a belly full of blood. As in so many things, proper planning prevents poor performance.  [Read More & Listen to the podcast]

Non-traumatic Subarachnoid Bleeds - A ton of things need to be done in a very short time in these critically ill SAH patients. [Read More & Listen to the podcast]

I would love to hear your comments and any suggestions for future topics.

My Podcast Alley feed! {pca-51f7db31b24ffbd03c05a2769a4aaf34}

Hi folks,

Sorry about the voice–got a cold off those damn ED keyboards

Thanks to my friend Reuben, this week we’ll talk about the asthmatic patient that codes while on the vent

The DOPE mnemonic gives you a path to figure out why a patient is desaturating

(If anyone knows who created the DOPE mnemonic, please add a comment or send me an email.)

If the pt is asthmatic, add an “S” to make DOPES

The “S” stands for Stacked Breaths–and it’s the first thing to address.

Address it by disconnecting the vent circuit. Don’t think about it, don’t dither, just disconnect the vent.

“E” is for equipment. Attach a BVM hooked up to O2 and you’ll eliminate ventilator equipment failures.

“D” is for tube displacement. Verify the tube with ETCO2, either qualitative or quantitative.

“O” reminds you to check for obstruction of the tube. See if you can put a suction cath all the way down.

If all of these don’t fix the problem, then consider “P” for pneumothorax.

Lung sounds are not always definitive. Throw on the UTS if you have the time.

Otherwise perform bilateral finger thoracostomies. What the hell is that, you say?

Listen to the podcast.

Then you can read more about it in this article

Tech Code (please ignore) YQAVYRPWGPHA

Don’t intubate the severe asthmatic,

try NIV first

continue the nebs on the NIV

obviously they need steroids and throw in Mag

does ketamine work? maybe…

If you intubate, Ron Walls says add lidocaine to your sedative and paralytic

if you put them on the vent make sure your plateau pressure stays below 30 cm H20

or make sure the flow graph shows flow has stopped before the next breath

Here is the vent lecture:

“Not the Greatest Vent Lecture Ever”

Hey folks,

If you are visiting from EMEDhome, Welcome to the EMCrit Blog. You may like some of our other ED Critical Care educational offerings, check out everything at the home page at blog.emcrit.org

This is the demonstration video for the Laryngoscope as a Murder Weapon Talk.

If you’d like to read the article in press at the Journal of Emergency Medicine, click here.

Here is the video:

Thanks to my friend and colleague Elmer Siong.

Chris Nickson is an Aussie, oops Kiwi, who is a lead author of a great blog: lifeinthefastlane.com and tweets under the moniker @precordialthump; check him out, he’s doing really good stuff. He wrote a comment about the last podcast–

Hey Scott,

Great to hear your views and approach to EGDT. I agree with the need for aggressive resuscitation of the septic patient – with fluid, antibiotics, vasopressors (we’re a ‘norad/ norepi shop’ too) and adequate oxygen delivery being the mainstays – and, if nothing else, the Rivers paper deserves credit for bringing this into the spotlight.

However, the Rivers study itself is still a cause of concern for me – a single center study that has never been repeated as an RCT, with a very high mortality in the control arm (mid-40s%), and more recently the WSJ allegations about about methodological ‘dodginess’ behind the scenes and concerns about conflicting financial interests (of which I’m not sure what to make).

Most ICUs in Australia don’t use CV02 monitoring, yet our mortality rates are substantially better than the Rivers study (ICU sepsis mortality around 20% these days, down from 34% in 1997) – different populations or something else? I’m also uneasy about the blood transfusion phase of the Rivers protocol. Hopefully trials like ARISE and ProCESS will help clear up what actually works. In the mean time, I heed your call to resuscitate!

Cheers,
Chris Nickson
ED/ICU Registrar, Perth

So in this brief aside, I respond to Chris’ comments and tell you a bit about the EMCrit Podcast EBM philosophy.

Here are the links mentioned:

• Henry Ford Hospital Reply to WSJ – 10.27.2008
• New MSSM ED Crit Care Sepsis Protocol

• MR of Early Quantitative Therapies for Sepsis

Hi all–Sorry for the delayed posting, but I just moved to a new apt.

In this episode I rant and rave about why for the most part Emergency Medicine has disappointed me by not doing something about our sick septic patients.

If you are offering aggressive therapy in the ED, then good on you.

Of course everything in this talk stems from River’s seminal work: EGDT Study

On this podcast,

I recap from last show, especially the concept of bare minimum normotension (called erroneously permissive hypotension by just about everyone else) and why we should keep the MAP higher if there is suspected elevations in intracranial pressure

I then talk about massive transfusion. This is probably the best strategy for a patient that will require greater than 8-10 units of PRBCs.

What may be the best review of the topic is by Spinella and Holcomb:

(Blood Reviews 2009;23:231-240)

I talk about

• 1:1:1 transfusion
• PCC, Factor VIIa, Cryo
• Calcium
• IV Access

coming up in the next few podcasts: Sedatives for Intubation, Trauma Airway Management, The Crashing A-fib patient

for some reason, the audio did not make it to itunes, this should fix it.

Thought we’d talk about some trauma stuff, specifically the resuscitation of the critically ill hemorrhagic shock patient.

There is much to discuss, so this will be a multi-episode affair.

Today, we’ll concentrate on the Lethal Triad and BP Goals.

Lethal Triad

The picture says it all.

Bleeding causes acidosis, hypothermia, and coagulopathy. Then the cycle begins as they all beget each other. If this continues for too long, it is irreversible.

We can iatrogenically make things worse by keeping our patients exposed and infusing ice cold fluids and products. By diluting their existing clotting factors and platelets with too much fluid and red cells. And by not ensuring adeqaute perfusion to counter acidosis.

BP Goals

Your goal is a MAP of 65. This is not hypotensive resus, which is still not proven. It is normotensive resuscitation; beyond 65, no additional benefts will be seen, but you do risk increased bleeding and dilutional coagulopathy.

If MAP < 65 – give fluids/products

If MAP > 65 – check perfusion

there are monitors for this such as NIRS measurement of thenar eminence, but at this stage, I recommend using the presence of a nice strong pulse and warm hands.

MAP > 65 & Good Perfusion-stand tight

MAP > 65 & Bad Perfusion-give fentanyl 20-25 mcg

why fentanyl? b/c taking away pain and fear will limit endogenous catecholamines and the pt’s bp will drop slightly from vasodilation. Now give fluids/products to take the MAP to > 65.

Here are the articles

resus of crit ill trauma patients

damage_control_anesthesia

Next Time: Massive Transfusion Protocols

The management of severe ETOH withdrawal and Delirium Tremens:

1. Consider alternative diagnoses

Here is my DT protocol

2. Start treatment with diazepam

3. If you reach 200 mg, switch to phenobarb or intubate and give propofol

4. Your goal is to get your patient sleepy, but arousable with a HR<120

Find Dr. Lewis Goldfrank’s lecture here

The citation for the CCM article is (Crit Care Med 2007;35:724)

I also discuss a listener email regarding succinylcholine and whether it causes increased oxygen consumption.

In short: Roc Rocks and Sux Sucks! (that one is for you Reub)

Mohamed, a listener from Sudan, emailed asking about the treatment of acute pulmonary edema in patients with low blood pressure. This is in distinction to SCAPE patients (see podcast 1).

If the patients have pulmonary edema and low BP from a cardiac cause, then they are in cardiogenic shock.

First, consider the etiology:

• Rate-related
• Valve Disorder
• Ischemic (Right sided infarct, STEMI, NSTEMI)
• Cardiomyopathy
• Toxicologic

At the same time, you are treating the patient with:

• Inotropes (dobutamine, milrinone, calcium)
• Pressors to achieve a MAP > 65 (allows coronary perfusion)
• Oxygenation support, most likely with intubation
• Optimize O2 carrying capacity (Hb>10)

Does the EM ban on letting sick patients go to CT scan make sense?

listen to the podcast and then register your opinion.

This week’s podcast is on the management of a the patient with SAH. It’s not a complete review, just some tips and reminders.

Best article for EM that I’ve found, comes out of Columbia

For more reviews on mostly ICU issues see here and here.

1. Get a neuro exam before you intubate

2. Intubation

Give pretreatment, now just lidocaine and fentanyl

Etomidate or propofol; plus sux.

Most experienced intubater should perform laryngoscopy

3. Treat Pain

and if intubated, give sedation

4. Treat Vasospasm

give nimodipine 60 mg PO or NGT

5. BP Control

place a-line

treat pain first

Give Labetalol or Nicardipine to achieve the patient’s baseline BP if the patient has good mental status

if they are obtunded, be a bit more conservative until ICP monitoring is in place

If MAP is below 80, give fluids, pressors, and inotropes

6. Anti-seizure prophylaxis

Load with phenytoin or fosphenytoin

7. Anti-fibrinolytics

Amicar is the main one these days; ask your neurosurgeon/neurointensivist on a case-by-case basis

see ehced.org for drip sheets

8. Reverse Coagulopathy

9. Think Heart

these patients can get EKG changes, dysrhythmias, LV stunning, and frank infarcts from their SAH

10. ICP ASAP

get the neurosurgeons to get the EVD (external ventricular drain) aka IVC (intraventricular catheter) in place as soon as possible

keep ICP < 20 and CPP > 55-60

Please Subscribe and Please Comment!

.

Hi folks,

this podcast is really brief–I gave a lecture at Jacobi last week (thanks for having me Jacobites!), and in response to a question I gave this rant on my vision of sedation after intubation.

Finally a non-intubation topic!

Bolus dose pressors and inotropes have been used by the anesthesiologists for decades, but they have not penetrated into standard emergency medicine practice. I don’t know why. They are the perfect solution to short-lived hypotension, e.g. post-intubation or during sedation.

They also can act as a bridge to drip pressors while they are being mixed or while a central line is being placed.

Click Here for printable sheet with mixing instructions

Ephedrine

I don’t use this one much anymore, listen to the podcast to hear why.

Onset-Near Instant

Duration-1 hour

Mixing Instructions:

Take a 10 ml syringe with 9 ml of normal saline

Into this syringe, draw up 1 ml of ephedrine from the vial (vial contains Ephedrine 50 mg/ml)

Now you have 10 mls of Ephedrine 5 mg/ml

Dose:

1-2 ml every 2-5 minutes (5-10 mg)

No extravasation worries!

Epinephrine

Do not give cardiac arrest doses (1 mg) to patients with a pulse

Has alpha and beta-1/2 effects so it is an inopressor

Onset-1 minute

Duration-5-10 minutes

Mixing Instructions:

Take a 10 ml syringe with 9 ml of normal saline

Into this syringe, draw up 1 ml of epinephrine from the cardiac amp (amp contains Epinephrine 100 mcg/ml)

Now you have 10 mls of Epinephrine 10 mcg/ml

Dose:

0.5-2 ml every 2-5 minutes (5-20  mcg)

No extravasation worries!

Phenylephrine

Phenyl as a bolus dose is just the best! It is clean, quick, and never causes trouble.

It is pure alpha, so no intrinsic inotropy, but increases in heart perfusion can improve cardiac output.

Onset-1 minute

Duration- 20 minutes

Mixing Instructions:

Take a 3 ml syringe and draw up 1 ml of phenylephrine from the vial (vial contains phenylephrine 10 mg/ml)

Inject this into a 100 ml bag of NS

Now you have 100 mls of phenylephrine 100 mcg/ml

Draw up some into a syringe; each ml in the syringe is 100 mcg

Dose:

0.5-2 ml every 2-5 minutes (50-200 mcg)

No extravasation worries!

Please send me any comments or questions

We’ve had a  few gruesome airways in patients with GI bleeds and bellies full of coffee ground emesis.

This is a top 10 list encompassing my approach to this difficult situation:

1. Empty the Stomach

Place a salem sump and suck out all of the stomach contents.
Varices are not a contraindication (see: Digest Dis 1973;18(12):1032 and Anesth Analg 1988;67:283)

Administer Metoclopramide 10 mg IVSS

2. Intubate the Patient with HOB at 45°

Semi-Fowler’s position will keep the gastric contents from moving up the esophagus

3. Preoxygenate like mad

You do not want to bag these patients, give yourself a preox cushion

4. Intubation Meds

Use a sedative that is BP stable, use reduced doses.

These patients NEED paralytics. You need to optimize first pass success. Paralytic agents actually increase the lower esophageal sphincter tone (Br J Anaesth 1984;56:37).

5. Gather your equipment to optimize first pass

Use fiberoptic laryngoscopy if you have it (e.g. Glidescope)

At the bedside, have a bougie, an LMA, a meconium aspirator (more below), and 2 suction set-ups

Wear eye protection!

6. If you need to bag after a failed attempt…

Bag gently and slowly (10 times a minute)
Consider placing an LMA if you need to bag.

7. If the patient vomits: Trendelenberg

This potentially keeps the emesis out of the lungs

8. Meconium Aspirator

If the normal suction is too slow, attach the meconium aspirator to your ET tube and the suction tube

9. No ABX for Aspiration

Aspiration in the initial phases is a chemical pneumonitis, not a bacterial pneumonia

See Marik’s article (NEJM 2001;344(9):665)

10. SIRS

Expect a sepsis-like syndrome from the aspiration. This folks may need pressors and tons of additional fluid

The video for this lecture is up at this link.

Awake intubation can save your butt.

It requires forethought and humility–you must be able to say to yourself, “I am not sure I will be able to successfully intubate this patient.” However, the payoff for this thought process is enormous. You can try an intubation in the ED with very few downsides. If you get it, you look like a star, if you don’t you have not made the situation worse.

Two of my critical care resident specialists, Raghu Seethala and Xun Zhong, volunteered to intubate each other awake. The purpose of this was to let them gain experience, understand what their patients would feel during the procedure, and to prove that awake intubation can be done without complicated nerve block injections or fragile equipment, such as a bronchoscope.

Here is the procedure for ED Awake Intubation–EMCrit Style:

DRY THEM OUT (Do All)

If you can give it early 10-15 min before topicalizing, it will be most effective.

• Glycopyrolate: 0.2 mg IVP (No central effects – does not cross BBB. You can use atropine, but more side effects are possible)
• Suction and then pad mouth dry with gauze – you want the mouth very dry!

TOPICALIZE (Do All)

• 5 cc of 4% lidocaine nebulized @ 5 liters per min
• Gargle with viscous lidocaine (4% best, 2% ok). Place a blob (~3 cc) on a tongue depressor, put it in the back of the throat and have the patient gargle and then spit
• Spray the epiglottis, cords, and trachea with 4% lidocaine (3 cc) in a Mucosal Atomizer Device (MAD). The patient will cough during this spraying, wear eye/face protection
• Have another syringe loaded with 4% lidocaine to spray with during the procedure

Note: the systemic and pulmonary absorption from this method is quite low. The only place to watch out is spraying the trachea. I would not spray more than 2-3 cc down the ol’ windpipe.

SEDATE (Choose one!)

• Ketamine and propofol in the same syringe makes Ketofol. The classic mix is 50 mg of ketamine to make 5 cc and 50 mg of propofol to make 5 cc. Put these both in a 10 cc syringe and shake. Depending on the patient’s hemodynamics, I sometimes will use more ketamine (75% instead of 50%). Give 1-2 cc every minute until you have the patient relaxed, but still breathing and arousable.
• Ketamine alone also works just fine. Start with 20 mg and give 10 mg every minute or so.
• If you have it, Dexmedetomidine also works very well as long as your patient is not bradycardic.
• If you have neither of these 2 mg of midazolam will do just fine.

• Preoxygenate with NRB

• Optimally position (ear to sternal notch) with the head tilted all the way back

• Restrain both arms with soft restraints to prevent the “grabbies”

• Switch to nasal cannula

• INTUBATE with Fiberoptic laryngoscope and bougie

• If the patient coughs or is uncomfortable after placing the bougie through the cords, push the remainder of the ketofol syringe.

• Thread  the tube over the bougie with the laryngoscope still in the mouth

• Confirm tube placement

That’s all for this week

For more info on awake ED intubation, you can view a complete lecture here

Thanks to Raghu and Xun for risking their singing careers and to Jimmy & Anita for technical support. *
The opinions on this site and in the video represent the author’s and not the opinions or policies of the Mount Sinai School of Medicine or Elmhurst Hospital Center. It is not my intention to provide specific medical advice for any individual patient. Please confirm anything on this video with your own clinical judgment and the policies and procedures of your institution. This video is for education purposes only; it does not represent a standard of care or clinical advice.

Sorry about the voice–blame the swine flu.

Case

Thanks to Joe Chiang

Severe DKA; Obtunded with pH 6.65, PaCO2 18, Bicarb 5
Pt’s mental status is worsening
The decision is made to intubate

Should you give NaBicarb?

Probably won’t help as patient is already breathing at their maximum. Unless they blow off the Bicarb-generated CO2, they won’t increase their pH significantly.

What you need

Properly fitted NIV mask
Ventilator, not a NIV machine
Someone who knows how to work the vent
Normal intubation stuff
If available, Quantitative ETCO2

Procedure

• Place pt on pseudo-NIV

Settings are
Mode Volume SIMV
Vt 550 ml
FiO2 100%
Flow Rate 30 lpm
PSV 5-10
PEEP 5
RR 0

• Attach ETCO2 and observe value
• Push the RSI Meds

• Turn the Resp Rate to 12
• Perform jaw thrust
• Wait 45 seconds

This violates the tenets of RSI, but keeping the pt alive is probably more crucial right now.
Most experienced operator should intubate the patient

• Attach the ventilator
• Confirm tube placement by observing ETCO2
• Immediately increase Respiratory Rate to 30
• Change Vt to 8 cc/kg predicted IBW
• Change Flow Rate to 60 lpm, this si the normal setting for intubated patients (forgot to mention this in the audio)

Why 30 BPM? Listen to the podcast.

• Make sure ETCO2 is at least as low as it was when you started
• Check ABG
• Pat yourself on the back

I did a spot on ETCO2 for Amal Mattu’s podcast a couple of weeks ago. I try to clear up some of the myths on the use of ETCO2.

Of course the most pervasive and potentially dangerous myth is that ETCO2=PaCO2.
Long story short, in our patients, it doesn’t.

Listen to the podcast for more…

Here it is, the 1st EMCrit podcast.

It’s on the topic of Sympathetic Crashing Acute Pulmonary Edema (SCAPE).

To boil it down to 10 seconds:

• Start patient on Non-invasive ventilation with a PEEP of 6-8; quickly titrate to a PEEP of 10-12.
• Start the patient on a nitroglycerin drip. Administer a loading dose of 4oo mcg/min for 2 minutes (120 ml/hour on the pump for 2 minutes with the standard nitro concentration of 200 mcg/ml.) Then drop the dose to 100 mcg/min and titrate it up from there as needed.

By 10 minutes, your patient should be out of the water.

See EMCrit.org for the references.

Please leave comments and tell me what you think.

-Scott

In which I introduce you to me and explain what this whole thing is about.

(better late than never)