Must-Read Resuscitation

Folks,

I know I am incessantly encouraging people to follow Dr. Smith’s EKG blog, but the most recent post is too good to not tell you all about. In it, there is a write up of a fantastic resuscitation.

Highlighted in it are double-defibrillation, Head up CPR, hypokalemia bolus dosing, ultrasound for stemi and VFib (!), esmolol bolus for refractory vfib,  cath lab availability and MDM, hypothermia discussion, and prognostics in cardiac arrests.  I mean, this case report has it all, and it is referenced and discussed for our enjoyment.  Read it.

The resuscitation you wish you had run IS HERE!

Read it. I’ll buy you a drink if you do.

Zach

Sepsis-3

I’m sure you guys have heard about the new sepsis definitions unveiled at the SCCM conference last week which were originally published in JAMA (2016;315(8):801-810); if not you’re in luck because I’ve outlined them for you below.  Keep in mind the sepsis definition has not been updated since most of you were still in high school- or middle school- I’m showing my age, in 2001, with Sepsis-2.

Sepsis-3:

New Terms and Definitions

  • Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection
  • Organ dysfunction: Acute change in total SOFA score ≥2 points consequent to the infection
  • Identification of patients likely to have poor outcomes:
    • ICU Patients: SOFA score ≥2: Overall mortality risk of approximately 10% in a general hospital population with suspected infection
    • ED patients: qSOFA score >2 (SBP < 100 mm Hg, RR > 22, or altered mental status)
      • These patients are likely to have a prolonged ICU stay or to die in the hospital
    • Septic shock: Sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 and a serum lactate level >2 mmol/L despite adequate volume resuscitation
      • Hospital mortality is in excess of 40%
    • The term “severe sepsis” has been abandoned

Better to be lucky than good

I was called to a code in the ICU.  I roll into the room, 38yo IVDA hx, admitted for sepsis, septic emboli, and ARDS.   Stable vital signs 10 minutes previously, now in PEA arrest.  Already tubed and had a triple lumen in the IJ.   Not a whole lot for me to add for immediate stabilization with a secure airway and access.   Already had epi x1.  Accucheck was 149 (never, never forget this in a code).

So I immediately get to go to the second phase and start thinking reversible causes.  With that hx, all sorts of interesting diagnoses on the playing field.  The one major thing I notice was the patient was extremely cyanotic from the upper chest on up.   CBC and BMP from a few hours ago essentially unremarkable aside from a white count of 26.  Coags normal.  Actually starting to kick around the idea of empirically thrombolyzing this dude.  All of a sudden, quick run of v-fib, zap him with 200 and voila! we have a pulse.  I order a new rainbow of labs, cxr, call his pulmonologist to recite my efforts,  and strut back down stairs with a little gangster lean feeling pretty good.

I sit down, take a deep breath, and head to see the next patient.  And BOOM!  Code alarm goes off once again.  Head back into the room, next verse same as the first.  Guy suddenly went PEA arrest again, CPR was already in progress.  No labs back.  I have them pull up the CXR.

IMG_3103

Well sh*t, I swear I listened to him during the first code.  Bilateral breath sounds (course, but there).   I listen again, knowing there is a big pneumo, still can hear.  Obvious tracheal deviation on the CXR, but time to get moving.   So I ask for an angiocath and a chest tube set up.  Deer in headlights, no one moves.  Someone finally scurries off to find a pleurovac and tube.

Still waiting for an angiocath, they hand me something that looks like something I’d LP a 10 day old with, not gonna cut it.  Finally they roll in with this kit that looked like they pulled off a dusty shelf.  Has what looks like a 8 inch spinal needle with a pigail catheter already attached to it.  That’s it.  nothing else in the kit besides and adaptor to attach to the pleuravac.  Don’t have a lot of time to search for anything else so I went with it.  Was actually really slick- put the needle into the chest cavity, pulled out the inner cannula, heard the hiss and fed the pigtail.  That’s it, working chest tube in place in about the same time it would take to do a needle decompression.

IMG_3105

Immediate return of pulse and stable blood pressure.   Thank god.  That would have been a totally reversible cause of death in a young patient.  If I hadn’t ordered or remembered to check that x-ray, would have been on my shoulders.

I post this for a couple of reasons.

#1 Don’t get too cute in your codes.  Start with the basics and build from there.  I was too busy thinking about lytics etc, and had an easily reversible cause right in front of me.  Don’t forget your DOPES mnemonic for ventilated patients.

D- dislodgement, check your tubes, end tidal or even preferably direct visualization.  Especially in a patient getting CPR.

O- obstruction, always suction, mucous plugging is an easy removal.

P- Pneumo, already talked this through.

E- Equipment, I recommend always pulling your codes off the vent and bagging through the ET tube to take this one off the radar.

S- stacked breaths.  Too much PEEP or high respiratory rates without adequate expiration time can cause air trapping and decreased venous return.  Once you pull someone off the vent and bag.  Take a second and manually press the chest wall down.  Can fix the problem immediately and you look like a total ninja if it works.

2015 ACLS GUIDELINES

The new 2015 ACLS guidelines were published this month!  I love new guidelines!  I’ve highlighted the important drug stuff (you guys are on your own for the rest).

Vasopressin: REMOVED FROM ALGORITHM: This was no surprise to me as vasopressin has never been shown to offer any advantage over epinephrine in studies to date.

“Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest (Class IIb, LOE B-R)”

“Vasopressin in combination with epinephrine offers no advantage as a substitute for standard-dose epinephrine in cardiac arrest (Class IIb, LOE B-R)”

Steroids: I’ve been skeptical of the use of steroids in cardiac arrest since 2009 inhospital cardiac arrest trial (steroids were combined with a vasopressor bundle or cocktail of epi and vasopressin).  Will need much more convincing data before I’ll recommend routine use- and that is exactly what our guidelines endorse as well.  Because: no one in the ICU dies before receiving a course of steroids.  The pre-hospital use of steroids is pretty clear: no benefit.

“In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post-arrest hydrocortisone as described by Mentzelopoulos et al may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy (Class IIb, LOE C-LD)”

“For patients with OHCA, use of steroids during CPR is of uncertain benefit (Class IIb, LOE C-LD)”

Epinephrine: Nothing groundbreaking here.  A few trials did demonstrate ROSC advantage with high-dose epi over standard dose; however, no improvement in survival to discharge (emphasis on good neurologic recover) over standard dose.  There is much concern with adverse effects of higher dose epi in the post-arrest period which may negate potential advantages during intra-arrest period.

“Standard-dose epinephrine (1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest (Class IIb, LOE B-R)”

“High-dose epinephrine is not recommended for routine use in cardiac arrest (Class III: No Benefit, LOE B-R)”

Antiarrhythmics: Really no changes.  Emphasized use of amiodarone over lidocaine (which is not new).

“Amiodarone may be considered for VF/pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B-R)”

“Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD)”

“The routine use of magnesium for VF/pVT is not recommended in adult patients (Class III: No Benefit, LOE B-R)”

Circulation 2015:132:S444-64

A-fib with RVR + sepsis + hypotension = conundrum

How do we slow the rate without lowering the BP? Will slowing the rate even help the BP? How do we raise the BP without speeding up the rate?

The patient who inspired this post came in for a bowel obstruction. Cards was initially consulted for possible new a-fib, but there really wasn’t much to do from a cardiac standpoint. THEN he perforated his bowel and went for emergency surgery, where he required pressors and went into a-fib with RVR. He was packed open and taken to the SICU, where he was hypotensive to SBP 70s, tachycardic to 160s, and intermittently hypoxic.

If you want to skip my thoughts on the case and head straight for the facts, here is an interesting article about a-fib in critically ill patients. It talks about the various options for management and the pros/cons of each.

If expert opinion is more your style, try this.

Of course, there is also controversy around slowing down a-fib when it is caused by sickness. Should we let the body do its thing to try and compensate? Here’s one article that suggests maybe we shouldn’t get so hung up on rate control in sick people.

Now back to the case. The surgery resident and I were of the mind that slowing the rate and organizing the rhythm should help with cardiac output. There are several reasons why this logic still seems to be in the majority.

– With a-fib you lose atrial kick. That little extra oomph from the atrium may not seem like a big deal, but it can have a significant impact on cardiac output. Here’s a fun article from 1965 that shows a 53% increase in cardiac output from converting a-fib to sinus (using quinidine because 1965). The results have obviously been redemonstrated in more recent studies, but how often do you get to reference quinidine? Not that often.

– Diastolic filling is important for stroke volume. With any tachyarrhythmia, less diastolic filling time means lower stroke volume. However people who do “math” would argue that increasing the rate would likely keep cardiac output about the same. This logic holds up with regular rhythms, but studies show that irregular rhythm decreases cardiac output compared to regular rhythm. Here’s one such study.

– In real life, we went for amiodarone and electrical cardioversion. From the a-fib in critical care article above, it seems like that’s still the best option.
Here’s a good article I wish I had read before embarking on a cluster of a cardioversion. P.S. Put the pads on correctly. Anterior-posterior pads definitely worked better for this 350 pound patient. Anterior pads = fail x3. AP pads = success!

– It’s worth noting that this is not one of the scenarios when you’re worrying about giving someone a stroke with cardioversion. This guy’s risk of death was much greater than his risk of stroke.

Another consideration for this situation was the choice of pressors. Eventually the patient ended up maxed on pretty much all pressors, but that may not always be the case.

Surviving Sepsis guidelines are all about Levophed as a first line pressor, which is usually a great option. But guidelines are just guidelines. How many of our patients are otherwise 100% healthy and just have a little sepsis? Not that many.

– In this case, I think phenylephrine may have been a better first option. Pure alpha agonist activity vasoconstricts without Levophed’s cardiac effects, which probably didn’t do us any favors with the RVR.

– Based on the EMCrit blog above it also seems like phenylephrine might have allowed us to use a beta blocker without worrying about blocking the effects of the pressor or a calcium channel blocker without exacerbating hypotension. Thoughts?

– Anyone have other ideas about pressors in this scenario?

There was a lot more to the case after that, but this post has already ended up way longer than I intended. In the end, it was a 350 pound unhealthy guy with a less than ideal heart, so unfortunately, his family ended up withdrawing care. I doubt anything we could have done would have changed his outcome, but maybe there’s something to learn from it that will help someone else someday. I’ve talked to several people about this case and gotten different opinions from each one, so I figure why not open it up for a few more opinions to really confuse clear things up.

Everything including the lipid sink

80+ yo gentleman with PMH of COPD, CHF, CAD, CKD, initially hospitalized for urosepsis and NSTEMI with a worsening AKI, and baseline CKD. Tuned him up and sent him to the floor where he accidentally received an overdose of his carvedilol. Got the call that the patient was hypotensive to 70s systolic, bradycardic to 30s.

Immediately pacer pads were placed to ward off evil spirits
-Started with 1L crystalloid bolus –> no response and with risk factors and pmhx, didn’t want to fluid overload
-Tried atropine (3-4 doses) –> no response
-Tried glucagon 50mcg/kg loading dose followed by 3mg/hr infusion –> still no luck and exhausted all the glucagon in the pharmacy
Running out of options here. I remember reading an article in Annals about using lipid infusions in beta blocker overdoses and figured it was worth a shot.

Started 20% Intralipid bolus through central line at 1.5ml/kg followed by 0.25ml/kg/min for 30min. Maybe it was the lipid infusion or just the combined effects of everything but by 6am, pt’s BP and HR had improved to normal limits and he began talking again.
It was a nice result but one I couldn’t celebrate that much – within a week, patient decided to go to palliative care and that was the last I heard of him.

The Kitchen Sink

Fairly early into an overnight shift the radio goes off.  EMS is approximately 6min out with mid 30s male undergoing CPR. Per bystanders, the patient was going running from door to door, banging on doors and yelling for help. Shortly after being taken into police custody he was found to be pulseless. Had been undergoing CPR approx 10 min. King airway in place. No improvement with dextrose and naloxone.

The intern on and myself go to Room 9 to get set up. When EMS arrives about 10 minutes later, CPR is still ongoing and rhythm has been asytole/PEA throughout. The story remains consistent with him going from door to door yelling for help but now there is some variation as to whether he was cuffed and then lost his pulse, was found without a pulse, or if he got into a physical altercation with the neighbor and then lost pulse shortly after arrest. There are no signs of trauma and we elected to not invite additional chaos by calling a Level 1.

CPR is continued. King airway switched out for ETT. Accucheck 250’s. Central venous access and bilateral chest tubes placed with no rush of air or blood. Sats persist at 85% on vent, etco2 is in 60’s. He gets epi q3m. A dose of vasopressin and steroids. Istat has K 5.5. Lactate >20. Received 2-3 amps of bicarb. Received calcium. Upon rhythm checks he was primarily asystole except for 2-3 checks with a narrow pea that would not persist. Each time the ultrasound was placed on his heart there was no cardiac activity. My thought process at this time was that he was either excited delirium that I’m not going to be able to do much about or some kind of ingestion/overdose. We called pharmacy and asked for lipid emulsion. His ETCO2 had remained between 40-60 and we were about 40 minutes out from reported time of arrest. I decided if the lipids were unsuccessful that would be when we would call it.

They arrived about 15 minutes later and were infused. By now his etco2 had drifted down to 10 on the most recent pulse check. No changes occurred and TOD was called.

Ready for discharge?

Interesting case from my MICU month.  Pt is a middle aged  WM with hx of HIV, CVA presented to the ED with hypoxic respiratory failure and sepsis. Intubated in the ED and admitted to the unit. Pt self extubated few hours later in the MICU. Responded well to fluids, antibiotics and O2 nasal cannula.  Few days later, nurse d/c’ed his RIJ central line.

Within minutes,  pt became severely altered, O2 sats plummeted to the 60s and  bedside ultrasound showed significant air bubbles in the cardiac chambers.

What happened? When central line was removed, the wound site was not immediately occluded (with fingers, dressing with tape, etc). As pt inhaled, air traveled through the communicating conduit into the central blood vessel.

What to do now? Intubate for severe respiratory distress. Place pt in left lateral decubitus position and Trendelenburg position–prevents air from traveling to the pulmonary arteries causing airflow obstruction. Hyperbaric oxygen therapy, if you suspect cerebral embolism, as it decreases mortality.

The pt was intubated, placed on his side with bed tilted down. Did fine and transferred to floor the next day.

Just some thoughts on stroke management in the acute setting…

A couple months ago (during lecture), we had a discussion regarding tPA and acute onset of stroke. As you would expect, we discussed the indications, contraindications, etc of treating stroke with tPA. We also touched on the subject of our role in pushing tPA here at UofL.

Obviously as a stroke center, our stroke team is working around the clock- and as such, generally takes the ball on this one. However, when we are practicing outside of UofL, a stroke team is not always going to be available and ultimately the management will fall on us. Hence the discussion and considerations for us making the call or at least working towards that possibility in the future.

Coincidentally, at precisely the same time as this conversation, a small journal, based out of New England, with a primary focus on medicine, published three fine articles on a similar topic. These articles were focused on the treatment of stroke in  the acute setting.

As pertinent to this post, they explored the use of thrombolysis as well as mechanical removal of thrombus when said thrombus is located in a proximal vessel. Now I won’t pretend I can read, but for those of you who can- below, are links to two “previews” and one complete view of the above mentioned articles. Additionally, an audio file is embedded, containing a break down of the articles by Dr. Dave Newman, of the Mt. Sinai School of Medicine in the Department of Emergency Medicine, to be featured on a future episode of EM:Rap.

Ultimately, I guess the questions I have regarding this as a post on Room9er are as follows:

1. I believe the Stroke team has embraced these articles and to my knowledge (as of February) may have moved towards mechanical retrieval of thrombus in proximal vessels in appropriate candidates. If we are trying to move towards a more ED involved decision tree, what will we need to know and where will our policies stem from? At least as a concept. At this time, I have only heard us discuss tPA, but if we as a hospital are moving towards multiple modalities for treatment of acute stroke, should we not be discussing these as well?

2. With consideration of a 6 hour time frame to thrombus retrieval, what is our (UofL) policy on timelines regarding retrieval. (This is not reflecting any current policies, merely one parameter from one study.)

3. How much time is required from page to cath? This is undoubtedly a big question. What does it take to have a vascular team, NES team, etc ready do go. How will this influence our time of onset to treatment guidelines.

4. Outside of UofL, taking into consideration transit time, etc. how will this influence the management of stroke? Based on CTA availability, transit time, local resources, etc.

ESCAPE

EXTEND_IA

MR CLEAN

 

DSI

DSI works. Weingart’s original article was descriptive. Now he follows with a prospective observational study. I actually haven’t read the whole article yet because like a good book, I just don’t want it to be over. Everyone needs to read this.

Also we all need to quit being slackers on room9er. Lets try to get a few more posts in before the holidays hit us.

Expert central lines

Fall: it’s that time of year when the PGY-1s start holding down the MICU.

If your MICU experience is like mine, you’ll get a few texts on the overnight from the medicine PGY-3s asking for help placing central lines. I’d put in a couple subclavians in the OR as a medical student and the venerable (legendary) Jason Mann had shown me some tricks, but I was definitely nervous being the go-to person.

Found these great videos for EM docs on central line placement. Most of the videos I’d seen before were showing you how to identify landmarks and such – these are a level beyond that and offer some great information and tricks for more expert line placement. Worth watching about once a year through residency.

Here’s part 1. Just search for parts 2-5 if it’s helpful.

Golden Hour

Below is the LITFL summary of another look at the importance of early ABx administration in septic patients. Septic and especially severely septic patients should be taken to room 9, obtain blood cultures promptly, and initiate antibiotics as early as possible.

 

Ferrer R et al. Empiric antibiotic treatment reduces mortality in severe sepsis and septic shock from the first hour: results from a guideline-based performance improvement program. Crit Care Med 2014; 42: 1749-55. PMID: 24717459

  • This retrospective analysis of prospective surviving sepsis data of patients admitted to the ICU with severe sepsis found that delays in antibiotic administration resulted in a concomitant increase in hospital mortality. Though the results are compelling with a linear relationship between time to administration and hospital mortality discovered it is key to interpret this study with caution as the data are uncontrolled for the antibiotic administration to time metric primarily studied by this paper. Multiple potential confounders exist that might account for the observed relationship that should be studied prospectively. In the meantime it makes reasonable sense to administer antibiotics as soon as possible after the actual discovery of real sepsis.  
  • Recommended by: William Paolo

Acute Cardiogenic Pulmonary Edema

Here is nice summary post by FOAMed guru Anand Swaminathan with evidence-based discussion of the role (or lack thereof) for diuretics in acute pulmonary edema. Trust me it works. See also the first Emcrit podcast on the topic.

Bottom line: minimal role for diuretics in the pulmonary edema patient in extremis. This is not the mildly fluid overloaded patient with normal respiratory status, they can use a little diuresis once BUN/Cr are determined.

The Trauma-Stroke Eval

Middle age male brought into Room 9 s/p crush injury. The patient was reportedly crushed against a box truck and a wall for a short period, but no prolonged extrication.

He complains of LUQ chest pain, pleuritic in nature, and denies abdominal pain. He was ambulatory after the event. PMH only significant for HTN, otherwise no PSH, no allergies, and takes lisinopril and hydrochlorothiazide.

He is AOx3, moving all extremities, well appearing in Room 9, and acting appropriate. He goes for man scan as he did strike his head and although can give me all the details of the accident he reports LOC.

Upon return from the CT scanner his VS are stable, and is placed in a regular ED bed.  Image review revealed multiple rib fractures, and suspicious appearing spleen.  Radiologist confirms grade 1 spleen laceration, but no active extravasation, as well as bilateral rib fractures.

While evaluating another Room 9 patient, the nurse came to update me that the patient was now unresponsive and foaming at the mouth.  I told her to give Narcan, thinking it could be iatrogenic analgesia toxicity, and I would be right there.

I arrive in the room, and he does NOT look right. He is foaming at the mouth, the narcan certainly changed his pupil size when she gave it, but did nothing to his mental status. Sternal rub, nipple pinch, and ammonia capsule all failed to appropriately arouse him.  The trauma resident is now at the bedside as well and just as perplexed as this isn’t what I described on the phone. I call radiology ask them to re-check his CT head but they said no, they see nothing. I again re evaluate him and now he will move only his L side, and follow commands on the L side of his body.

Well…..crap, this is dysarthria R sided hemiplegia. Stroke paged, obtained stat CTA head and neck, and then straight to Room 9 to intubate him. See the CTA imaging below:

CTA

Carotid artery dissection…

He obviously is not a tPA candidate, but he did go for an intervention procedure with the stroke service.  He did have a clot retrieved, but I have visited him on the floor a few days later and he had no improvement.

He went on to develop cerebral edema as well and had a large hemicraniectomy. He also had an ex-lap for an increase in abdominal distension, and found to have pancreatic ascites (3L removed from the abdomen). The spleen did fine.

Looking back, his mechanism did not support a reason for him to dissect a carotid. He had no external signs of injury, he had no neck pain, my guess is he did have a whiplash type injury but again, not something I expected. In addition, this man had a normal neuro exam upon presentation, full strength, no numbness/tingling with the exception of reporting headache, which I thought was from him striking his head.

After a lit review, there are a few teaching points I want to highlight from this case.

Traumatic Dissection (carotid, vertebral, spinal arteries)

– consider it with hangings, significant head/neck trauma, hyper-extension injuries, lateral rotation injuries of the head, base of the skull fx, c-spine fractures(especially those with displacement or involvement of the transverse foramen,vertebral body), lefort fractures (types II and III), or seat-belt sign over the neck
– Sign/Symptoms vary greatly. Stroke like symptoms are concerning but can be as generalized as headache/migraine, neck pain, neck hematoma, blindness, aphasia, weakness/sensory loss, Horner’s syndrome, tinnitus, CN deficits, diplopia, locked in syndrome, ataxia, vertigo, dizziness

Dimer wins again

Here is a post from Ryan Radecki at EM Lit of Note. His philosophy mirrors what I took from Jeff Kline the PE guru on the approach to PE workup. When you have committed to ordering a CT-PA, then get a d dimer and if NEG, CANCEL the CT. Controversial of course. But the dimer is MORE SENSITIVE than a CT. Some say the d dimer is only for “low risk” patients, but check out this study using not necessarily low risk patients.