EMCrit Podcast 130 – Hemodynamic-Directed Dosing of Epinephrine for Cardiac Arrest

epi-pen

Today on the podcast, I address the last little bit from my SMACC lecture on the new management of the intra-arrest: hemodynamic, individualized dosing of epinephrine.

normanparadisadonehThe podcast is interspersed with clips from Professor Norman Paradis

Articles/Posts on Epinephrine by ACLS Guidelines

  • (15306666),
  • http://www.emdocs.net/epinephrine-cardiac-arrest/
  • http://www.jems.com/article/patient-care/new-resuscitative-protocol
  • (24846323)
  • (19934423)

Epinephrine Dosing Based on DBP

Three Swine Study

(Crit Care Med. 2013 Dec;41(12):2698-704)

(Resuscitation. 2013 May;84(5):696-701)

(24945902)
Here is the abstract from the latter study:

AIM: Advances in cardiopulmonary resuscitation (CPR) have focused on the generation and maintenance of adequate myocardial blood flow to optimize the return of spontaneous circulation and survival. Much of the morbidity associated with cardiac arrest survivors can be attributed to global brain hypoxic ischemic injury. The objective of this study was to compare cerebral physiological variables using a hemodynamic directed resuscitation strategy versus an absolute depth-guided approach in a porcine model of ventricular fibrillation (VF) cardiac arrest.

METHODS: Intracranial pressure and brain tissue oxygen tension probes were placed in the frontal cortex prior to induction of VF in 21 female 3month old swine. After 7minutes of VF, animalswere randomized to receive one of three resuscitation strategies: 1) Hemodynamic Directed Care (CPP-20): chest compressions (CCs) with depth titrated to a target systolic blood pressure of 100mmHg and titration of vasopressors to maintain coronary perfusion pressure (CPP)> 20mmHg; 2) Depth 33mm(D33): target CC depth of 33mm with standard American Heart Association (AHA) epinephrine dosing; or 3) Depth 51mm(D51): target CC depth of 51mm with standard AHA epinephrine dosing.

RESULTS: Cerebral perfusion pressures (CerePP )were significantly higher in the CPP-20 group compared to both D33 (p<0.01) and D51 (P=0.046), and higher in survivors compared to non-survivors irrespective of treatment group (P<0.01).Brain tissue oxygen tension was also higher in the CPP-20 group compared to both D33 (P<0.01) and D51 (P=0.013), and higher in survivors compared to non-survivors irrespective of treatment group (P<0.01).Subjects with a CPP>20mm Hg were 2.7 times more likely to have a CerePP>30mm Hg (P< 0.001).

CONCLUSIONS: Hemodynamic directed resuscitation strategy targeting coronary perfusion pressure>20mmHg following VF arrest was associated with higher cerebral perfusion pressures and brain tissue oxygen tensions during CPR. University of Pennsylvania IACUC protocol #803026.

Human Study by Dr. Paradis

Coronary Perfusion Pressure and the Return of Spontaneous Circulation in Human Cardiopulmonary Resuscitation

(10.1001/jama.1990.03440080084029)

Coronary perfusion pressure (CPP), the aortic-to-right atrial pressure gradient during the relaxation phase of cardiopulmonary resuscitation, was measured in 100 patients with cardiac arrest. Coronary perfusion pressure and other variables were compared in patients with and without return of spontaneous circulation (ROSC). Twenty-four patients had ROSC. Initial CPP (mean±SD) was 1.6 ± 8.5 mm Hg in patients without ROSC and 13.4 ± 8.5 mm Hg in those with ROSC. The maximal CPP measured was 8.4 ±10.0 mm Hg in those without ROSC and 25.6 ±7.7 mm Hg in those with ROSC. Differences were also found for the maximal aortic relaxation pressure, the compression-phase aortic-to— right atrial gradient, and the arterial Po2. No patient with an initial CPP less than 0 mm Hg had ROSC. Only patients with maximal CPPs of 15 mm Hg or more had ROSC, and the fraction of patients with ROSC increased as the maximal CPP increased. A CPP above 15 mm Hg did not guarantee ROSC, however, as 18 patients whose CPPs were 15 mm Hg or greater did not resuscitate. Of variables measured, maximal CPP was most predictive of ROSC, and all CPP measurements were more predictive than was aortic pressure alone. The study substantiates animal data that indicate the importance of CPP during cardiopulmonary resuscitation.

Good Review on Epinephrine

Epi Review

AHA Cardiopulmonary Resuscitation Quality Statement

by Meaney P. et al (Circulation 2013;128:417)

Metrics

  • CCF>80%
  • Rate 100-120
  • 5cm depth
  • Full Recoil
  • <12 BPM, Minimal Chest Rise

Monitoring/Feedback

  • Art/CVP CPP>20
  • Just Art Line DBP>25-30 (I disagree)
  • ETCO2>20 mm Hg

If DBP < 20 optimize compressions or vasopressors (Circulation 2011;123:e236)

CVP can be higher during the poor flow of the arrest state (3970745),(Am J Emerg Med. 1985 Jan;3(1):11-4.), and (3946853) and this one had a mean of 16 (10.1161/01.CIR.80.2.361)

so I would shoot for 35-40 mm Hg

Goal is to give less epineprhine

Hemodynamic-directed CPR Review

(24783998)

Now on to the Podcast…

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Comments

  1. Paul Bishop, NREMT-P, CCEMT-P says:

    I share your many opinions on epinephrine, and I love this podcast. With that being said, why are we not looking at using phenylephrine, either bolus or infusion(I like therapeutic steady-state infusions…) for cardiac arrest? Hmm…maybe I’m on to something…

    • Phenyl lacks alpha-2 which is believed to be more effective in the arrest state. Head to head were done and phenyl was no better than epi. Norepi makes a lot of sense, though those studies did not pan out either (all were super small). After we prove epi works in PARAMEDIC2, maybe you can do some head to heads vs. phenyl.

      • Craig Rosebrock says:

        Keep in mind that bolus of phenyl results in possible bradycardia… This is likely not a good idea in a crashing patient. When you get that drop in pressure for example after propofol during induction, you have to be careful that they are not brady and hypotensive….because if you push a dose of phenyl you could be in for a bad outcome…hence why anesthesia does not give a big slug of phenyl and uses little bursts… so I am not sure phenyl would be advantageous in a code. Some argue that this is “reflexive” however I have seen a drop clinically with bradycardic patients…they tend to drop regardless of blood pressure staying about the same…It should therefore not be used in my opinion if patients that rely on a heart rate dependent cardiac output. I guess it is hard to know what is going on in the crashing patient in terms of what is going to happen. But if the heart rate is in the low range and they have no pressure and you raise it just enough to induce some form of reflex, seems you could drop your HR too much.

  2. Victoria EM registrar says:

    Can you give us an idea of how you dose the adrenaline practically. Eg: DBP is 15 despite good compressions. What dose of adrenaline would you then give, ug/kg?

  3. Hey Scott awesome thought provoking podcast on Epi in CA!!! So I have some questions. First my service performs CCR w/ high flow NC oxygen for the first 4-5(1 round equals 200 compressions) rounds of CPR. So no ETCO2 measurements being done. During those first 4-5 rounds we are setting up for intubation that is well planned and choreographed with a VL device. Prior to that we have very little stoppage in CPR between each round when we switch out compressors and do a quick rhythm check as well(, then should we be breathing AT ALL before ROSC in cardiac arrest Pts prior to ROSC if PPV increases IT pressures and subsequently decreases CPP? And finally… 3. Do we absolutely know 100% that we are decreasing CPP with appropriate PPV in humans in CA? Thoughts to you and the community…?

  4. Great work Scott.

    Firstly I love your ‘outing’ of the current quality of evidence around intermittent dosing. We have agreed in the past that it’s essential that we know what our evidence base is for our current dogma before considering change. It looks as though the current evidence is weak at best and that arguably opens the door for us to consider other therapies and thoughts.

    I really enjoyed this very much indeed.

    I have one question for you though which I just know that you have already considered (you must have) but I did not spot in the podcast.

    If the theory is to maintain a coronary perfusion pressure AND you have an art line in…… could you/should you administer the adrenaline (that’s epinephrine in England ;-) ) as an infusion rather than as a bolus?

    I feel sure that you’ve considered this already and would love to hear your thoughts.

    vb

    S

    • Have thought of this my friend and agree it makes a lot of sense. I think the reason for the pushes is so you can see rapid results (~60-90 seconds) of your epi and know if you achieved your goal. I imagine we can work out an infusion that would do the same, but it would essentially be giving a bolus with a pump.

  5. Matt, yes we have evidence though I don’t have it at my fingertips. You should check in two places–first look at the work on excess resp rates during cpr and it should link to the evidence (esp. look at Dan Davis’ stuff) and then look at the impedance threshold device stuff, it should also have the links to higher thoracic press. decreasing venous return.

  6. Great stuff, Scott. Thank you. Now that you’re at Stony Brook, maybe you’ll get a chance to get a little HEMS involvement?

    We’ve got to keep in mind that when we’re using ETCO2 to monitor the quality of our resuscitation and prognosticate (and we should be), if the patient gets bicarb, the ETCO2 will be significantly falsely elevated, at least for several minutes, which can give us a false sense of security that things are going relatively well when they’re not. I know you’re not a big fan of empiric bicarb, but a little paper out of Carolinas (Littmann Med Princ Pract 2014; 23:1-6 A simplified and structured teaching tool for the evaluation and mgmt of PEA) has been getting a lot of press lately (EMRAP and Mattu’s EMCast) that will probably increase the use of empiric bicarb for wide-complex PEA.

  7. soren rudolph says:

    Hi Scott – how about doing adrenaline/epinephrine infusion and titrate to sufficient CPP? any studies or experience?

    • soren rudolph says:

      ….ups didn’t read the post above!!

      • Hi Soren, yep I had the same thought and the reply from Scott answers this.

        What was in my mind was the point in the podcast when SW was talking about increasing dosage to achieve a higher DBP if ROSC not obtained. In my head I had the idea of then increasing an infusion dosage (as with do with other vasopressors) as opposed to just increasing the dosage or frequency of boluses (which cognitively is probably harder to protocolise & achieve). I think the aim is essentially the same as SW says, but as a mechanism might be easier in practice.

        An infusion approach could allow you to set up an epi (that’s adrenaline for those over here ;-) ) infusion in advance of a patient arrival – connect and infuse on arrival as required and then titrate to effect.

        Also worth mentioning that we did routinely place subclavian central lines in cardiac arrest patients in the past. We used to do this routinely but less so of late. Currently we do not measure pressure through them, but that would be pretty easy to do.

        Lastly PARAMEDIC 2 study is here http://www.controlled-trials.com/isrctn/pf/73485024 & here http://www.nets.nihr.ac.uk/projects/hta/12127126

        It has just been approved for recruitment http://www.telegraph.co.uk/health/healthnews/11028692/Heart-patients-to-be-given-placebo-by-paramedics-in-controversial-trial.html so results will be a little time in coming but it does look like an effective design.

        Let’s hope it’s definitive!

        vb

        S

  8. Fantastic podcast Scott, which got me thinking that we’re maybe not as far apart on our intra-arrest management as I previously thought.

    Whilst, as we discussed, I’m not dosing adrenaline/epinephrine on intra-arrest diastolic BPs, I do target as high an intra-arrest BP as possible with my chest compressions. If the person doing chest compressions is unable to generate a decent pressure, I get them off the chest and replace them with someone more likely to get a higher pressure. (i.e. change a light 50kg nurse for a 100kg rugby player). I don’t have a definitive target, other than aiming for a “normal-ish” BP and trying to get the pressure higher if CPR is unsuccessful at a lower BP, much as Dr Paradis and you discussed. In this regard, I’m with you on a higher DBP than recommended in the Meaney paper, but use improved chest compression, rather than drugs, to target it (I’m still giving adrenaline, just not in your targeted manner).

    So we probably have a similar goal, just a different way of getting there. Hopefully the optimal targets, and methods to achieve these, will be clarfied in the near future.

    • YES! Improving compressions should be your first technique and the AHA paper advocates this as well. However, just as we can fill the tank in a septic pt with 10 liters of fluid or with 3 liters+a whiff of norepi; a whiff of epi may make good compressions even more effective

  9. Hey Scott,
    Hope you’re enjoying the new gig @ the new shop!
    This is awesome stuff- sounds like potentially revolutionary cardiac arrest care.
    It never made sense to me the random 1mg q3-5 mins dosing, and I’ve always been skeptical of it- glad to learn about the robust research behind that! Every other time we use pressors in resuscitation, dosing is always guided by a goal-directed approach, and I see no reason we should just go with blind dosing in the most fragile of patients (the arrest patient), especially given the great potential for deleterious effects of too much epi in these guys. You said you’ve generally found that when using this goal-directed approach that you end up using less overall epinephrine.. my only concern is that in certain circumstances, this could potentially, actually lead to increased epi administration, if compressions are deemed optimized(whether they truly aren’t, but even if they truly are) and estimated CPP continues to be lacking. I think one of the keys to any code is figuring out what the hell the etiology is, and I always use intra-arrest ultrasound as much as possible… I can’t help but think of things such as the concept of being “fluid-loaded” in the non-arrest pt and how that might apply to the arrest patient- and then how this may effect epinephrine dosing. Anyway, so glad to see you continuing to push the envelope on this stuff, and looking very forward to the future of cardiac arrest care.
    Sam

  10. Paul Bishop, NREMT-P, CCEMT-P says:

    I would like to see us using epinephrine infusions more in lieu of IV bolus epi during cardiac arrest, at least as long as we still continue to use epi on the regular. Mainly because it’s titratable.

  11. I have experimented with an intra-arrest epi infusion at 0.5 mcg/kg/min, which for our 100kg Americans is 50mcg/min, or the equivalent of 150-250mcg over 3-5 min, so 1/6-1/4 the ‘regular’ dosing of 1000 mcg every 3-5 min. This allows me to be on the side of the ‘epi-haters’ and still give some more appropriate dosing, similar to the doses I would use if ROSC was acheived and the BP was in the toilet and needing big doses of epi to maintain it.
    With an N of 1 in a massive PE case receiving 25 min of good quality CPR and Lytics following witnessed ED arrest the pt left the hospital neuro intact.
    Thank you England for doing the epi:no epi study!

  12. Great podcast Scott!

    Fantastic review that filled a couple of empty litterature and history slots for me. Completely agree with your approach which fits with a N=1 approach to tailoring therapy. I’ve been pushing our ED docs to use ETT or CPP but as you know, people like to consider acls as a gold standard and deviation to be heretical!

    Really looking forward to the NIRS data, as it is something I use (cerebral and somatic simultaneously) to titrate pressors in shock, with sometimes interesting results, basically finding the sweet spot between pressure and perfusion. I anticipate that’s what you guys will talk about, so happy to have more empty slots filled!

    Keep it up!

    Philippe

  13. J.Bishop says:

    Hey Scott,

    Thank you for yet another great podcast. I work in paediatrics so the idea of using ETCO2 levels to titrate epi administration sounds appealing as a) I am not sure quite what I would aim for as a cardiac perfusion pressure and b) getting lines during arrest is already a little tricky.
    My question is around the logistics of when to respond to changes though. I think of epi as being a cause for a decrease in ETCO2 levels during arrest due to the vasoconstrictive drop in pulmonary blood flow (increased dead space ventilation). The 2010 PALS guidelines describe this as being an issue for the 1 to 2 minutes following administration.
    When do you actually evaluate whether things have worked or not? If the ETCO2 is decreased when it’s “time for the next epi dose” is that because the patient needs more or because the PVR effects of the last round are still present.
    Thanks.

    • we usually give epi q5 minutes in my shop, so the time to assess is 5 minutes later from the epi. I think 3 minutes would be ok as well. By then you should see positive results of the epi if you are going to see them.

  14. Craig Rosebrock says:

    BANG BANG BANG

    Paradis nails it at the end in my opinion. The overall care is the issue in my opinion.

    I will give you my thoughts Scott.

    Dose of epi is important, but I think being prepared to handle the outcome is more important.

    As a critical care guy working in units all across the USA, I have developed a kinda of step by step when I do a code…obviously there are limits to this process…namely staff either lets me do this or not. For example, some places dont have stored lines in the floor code carts like in the ED or ICU. So it depends on the setting. But for the last several years, I usually order up an epi drip and an amio drip from the first moment I walk in the room. I do this because more often than not I end up needing them.. When all the drugs are on board as per acls, they usually have wicked arrythmias — especially if it was a long code. I know they are going to be at risk for possible v fib arrest despite what the initially insult was. I usually end up needing the epi drip because I know that once the epi wears off they are going to crash again. I tend to drop an introducer sheath in the subclav or if ultrasound is around, I use the neck or groin. I typically do not do A lines on crashing patients unless I really think I need one (maybe I will add that to stuff to do).

    I have watched over the shoulders of some physicians run codes and sat back since I was in their ED or somewhere else outside the ICU to see them struggle to get the drip drugs when they needed them. A good bolus of amio just prior to a defib seems to give me better results.. I have no studies, just what I have witnessed over the last 7 years since I got out of fellowship.

    I also do not like to see extensive codes with a few little 21 gauge needles in the foot. Inteross is comming around, but I tend to not use them unless i just cant get access which does happen but is rare. I think a good line and having my drips ready are very important. I think it is tragic when somebody does a good job in the field and in the ED, but then stops short of starting the appropriate drips. I think the good ED docs set me up for success while some set me up for failure… It has to be a team effort or a weak link will break the chain.

    I can say for a fact that in the non academic places I have worked, people sometimes march slowly along and do the action then reaction type of medicine.. oh gosh i need an epi drip.. ok thats now gonna take a few minutes to mix up as apposed to saying hey…I have been here before…I better have pharmacy get that drug ready. It is also sometimes the same with lytics..if you dont ask pharmacy to make it the second you get there, you maybe waiting a few minutes when you really decide now is the best time to use it. I see each patient as a human first…but I see the physiology as a complex chess game..the russian grandmaster sits across from me every single time I walk in the room. If you react only when he acts, you will be beaten every single time before you even move your first pawn. If you think ahead and play as if you have played with him a thousand times, you will be much more thoughtful and prepare for every possible move before lifting a piece.

    Also props for this website….i absolutely love it

    Craig

    • Craig–Great comments and I am of like mind. Only difference is I ask for a norepi drip and just give my amio by bolus, but exactly the same mindset. I am going to start asking for my norepi drip at the beginning of the code rather than at ROSC–it is a fantastic tip!

      • Fletch Schubert says:

        Why not start your epi. / norepi. gtt during during the code and bolus until you get the CPP up to goal?

        • Craig rosebrock says:

          When I am in the ICU with a patient I know, I will run the code a little different than then I am on the floor or in the ED assisting the ED doc. Usually when not in the unit I will do the standard acls pathway and at some point add the EPI drip. In the unit if they are on pressors already I essentially ask pharmacy to make the EPI once I see that the initially round of EPI had a positive result. I have been known the get the patient back and keep the EPI hanging but not running so I have it of they code again quickly. It wards off the bad omens.

        • you absolutely could. The doses of epi are 2 orders of magnitude higher than the norepi dosing we use with drips.

  15. Fletch Schubert says:

    Is there room for using a feedback loop such as this with Epi admin in a trauma code situation? This would be after obvious interventions were already performed, bilat. finger thoracotomys, endotracheal intubation, etc.

    • different physio in trauma. their problem is not going to be fixed by peripheral clampdown. they need their chest opened or their descending aorta blocked.

      • Craig Rosebrock says:

        Awesome point

        Too often people think that all hypotension needs pressors. Sometimes it is hard to convince the less experienced folks that the issue is not due to vaso dilatory shock. Pressors in tamponade or severely preload dependent patients can lead to a quick demise. You have to run a thorough differential in any shock slash code situation.

  16. SAMGHALI says:

    Dear Scott,

    I hope you are well my friend.

    After listening to your Vasopressor Basics cast, I came back to revisit this one. The more & more I think about cardiac arrest, what we do, and what our goals are, the less sense the idea of shooting for a higher and higher “perfusion” based upon whether or not we have attained ROSC makes. I am guessing the thought must be based on this notion: if we are not attaining ROSC with current measures, increasing perfusion more and more increases our chances of doing so— and I’m not sure that correlation bares out. If you look at CPR as simply a temporizing measure to keep the patient alive to buy us time to figure out the etiology of the code (and reverse it), then it would follow that our goal should be to simply provide “adequate” perfusion to the brain & heart during this “holding period” of CPR, and that failure to attaining ROSC doesn’t necessarily indicate that the perfusion we are generating with our chest compressions and pressor dosing is inadequate. Whatever numbers we are generating (whether it be End-Tidal, estimated CPP based on DBP, etc) may be completely sufficient. Therefore it seems almost silly to keep increasing our Epi dosing based on the fact that we haven’t attained ROSC, and to deem these pts to be “non-responders”. I say this keeping in mind the detrimental effects on neurologic outcomes w/too much EPI. If we think about the types of “codes”: “PEA” is it’s own different beast and entirely another conversation. In codes with shockable rhythms, clearly at least the immediate goal is to shock out into a perfusing rhythm, and increasing epi certainly may be completely counterproductive in this setting. In general, attaining & maintaining ROSC w/good neurologic outcome will be a result of maintaing perfusion during this temporizing period, but the ultimate goal would be reversing the etiology of the code. The other thought is that there are few code etiologies that epinephrine would be the mainstay of treatment/reversal for and in these settings it seems fluid administration/management would be crucial. You almost never hear this discussed. In the shock patient, we obsess over ways to figure out how to determine exactly how much fluid we need to give down to the drop, before starting the pressor agents. In cardiac arrest, we seem to just talk about Epi, Epi, & Epi.

    So is it a flawed paradigm that our markers of perfusion–whatever numbers we are looking at and using in our “goal-directed” strategy–necessarily need to increase (and along with that Epinephrine dosing) if no ROSC, and that this will augment our chances to attain and sustain it, and more importantly-to achieve intact neurological recovery?

    My thoughts,
    Sam

    My thoughts,??-Sam

    • really comes down to whether cpr is a temporizer for ECMO or an attempt to resuscitate. In the former situation just enough to perfuse is enough. If CPR is all you have then you need the pt to come back.

      • SAMGHALI says:

        I think CPR in general, like ECMO, is little more than a temporizer. Point is: perfusion via CPR may be adequate and lack of ROCS is not necessarily an indication that the perfusion (CPR) is inadequate. The mentality that “yet to attain ROSC” mandates “better perfusion” may be harmful, esp considering this will often lead to more intravenous epinephrine. We hope perfusing the heart (while perfusing the brain) will attain ROSC, but IMO the ultimate goal lies is ID’ing the etiology of the arrest- and reversing it.

        -Sam

        • I can agree with your intent, but not your execution. The reason ECPR exists is that you can rarely identify the cause intra-arrest and you can rarely treat an identified cause intra-arrest. Peri-arrest lytics are not a great answer, and aside from that we have little to offer except getting ROSC or going to intra-arrest PCI. Not really seeing the logical extension of your argument.

          • I think that we have more than just “little” to offer pts in cardiac arrest w/regards to reversal of etiology. We all know etiologies consist of more than just MI/PE,(and as you know I think it’s still worth a whirl even in these pts to give lytics a shot IF you have something hard to go on to suspect it, and you’ve done everything else). But there are all the rest of the H’s & T’s. (ie: Hypovolemia/hemorrhage,hypo-electrolytes, hyperK, hypothermia, tamponade, tension pneumo, OD’s, etc) I list these not to regurgitate basic ACLS, but bc I think these causes have an actual real, intra-arrest reversal. With regard to ECPR, deep down I truly believe in it (in the right pt), but as you know there is no good evidence in support of ECPR either.

            **But these aren’t even my argument at this point. My argument is: we don’t know the threshold at which perfusion produced by CPR is adequate. If A-Line is in, using estimated CPP (based on DPB and estimated CVP) makes a lot of sense. But whatever mechanism we do use to judge perfusion, there is no evidence that more is better. I don’t like the idea that “pt hasn’t come back yet, he/she’s a non-responder, and so we must keep aiming for a higher estimated CPP” — This will inevitably mean more Epi. This idea is especially worrisome for me in the pt who is in & out of a shockable rhythm, given the pro-arrhythmic effects of Epi, in which case it may not only decrease chances of shocking out, chances of ROSC, but more importantly intact neurologic status. Even in the scenario where there are no other identifiable reversible causes & we do nothing else intra-arrest other than produce perfusion via chest compressions & Epi, there’s no evidence that more and more perfusion will increase neurologically-intact ROSC. I am hopeful we can figure out where this threshold is with on-going Cardiac Arrest research in the near future.

            -Sam

            • Again, Sam you are arguing with theory. Extend all of the above to actualities. We take out all of the intervenable parts of H and Ts in the first 5 minutes of the arrest with ultrasound and empiric treatment.

              Since we actually use mechanical cpr, the compression efficacy of the rescuer is not part of the equation.

              So now you have about 20-25 more minutes to run a code after all of the above on the 60 y/o in front of you. So you are going to keep doing the same thing for that period of time and your contention is that something will change? Perhaps by improving the physiologic mileu? The differential blood gases between artery and vein when studied in arrest would go against this theory.

              I think we do need tiered interventions in these circumstances. Giving more and more epi very well may not be the answer, and it is not an answer I have given.

              Your discussion above re: fluid is not consistent with the hemodynamics of arrest. It increases CVP, increases Right sided dilation and causes massive pulmonary edema, but doesn’t affect outcome. We did this experiment on multi-thousand patients in NYC with the intra-arrest hypothermia study.

              The right answer will probably be REBOA/SAAP or some variant thereof.

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