Saturday, April 6, 2013

68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

The following is told with full permission of the patient, who is a paramedic who also started, owns and runs with his wife a company for teaching CPR.  He has taught CPR to over 100,000 people.  And he's a wonderful guy.   Here is his story:

Near midnight in December, this 56 yo very healthy and vigorous paramedic was out on a run with a critical case when his partner found him unresponsive in the front seat of the ambulance.  The partner began manual chest compressions immediately and called for help.  He was found to be in ventricular fibrillation and was defibrillated 4 times, unsuccessfully.  After a few minutes of manual chest compressions, the LUCAS device was applied.  Due to jaw clenching, he could not be intubated and so was ventilated with bag-valve-mask.  He received 1 mg of epinephrine and 300 mg of amiodarone and still could not be defibrillated. 

On arrival in the ED, he was in full arrest and undergoing LUCAS CPR.  He had been in arrest for 30 minutes at this point.  O2 saturations were 70% with a waveform.  He was given succinylcholine and intubated and the inspiratory threshold device (ResQPod) was attached to the end of the tubeSlow ventilations were guided by the timing light on the ResQPod.  Continous cardiac ultrasound revealed good cardiac contraction with each compression.  CPR was very briefly held and the rhythm was ventricular fibrillation with no ultrasonic cardiac activity. 

He was given 1 mg of epinephrine, 3g of calcium gluconate, 100 mEq of bicarb, and 100 mg of lidocaine.  At approximately 40 minutes (10 min in the ED), a 2nd mg of epinephrine (6th overall) and 2 g of MgSO4 were given.  The monitor confirmed V fib and he was defibrillated again, with conversion to sinus rhythm.  The LUCAS was paused.  There was good cardiac activity on ultrasound and strong pulses.

With successful return of spontaneous circulation, the cath lab was activated based on the presumption that this would be a coronary event (a greater than 50% probability even without a 12-lead ECG).

A 12-lead ECG was obtained:
Sinus tachycardia.  The QRS is very wide, with a right bundle branch block (RBBB).  The initial r-wave is replaced by a Q-wave in V1 and V2.  There is also left anterior fascicular block.  New RBBB + LAFB is a very bad combination and suggests a huge STEMI, either proximal LAD or left main.   

Is there ST elevation in addition to RBBB and LAFB?  To find out, you must find the end of the QRS.  In this case, it is best seen in lead V1, and if you draw a line down to lead II, which is across the bottom of the tracing, you can establish the end of the QRS in II.  Then you can find the end of the QRS is every lead, as below:
This is very similar to a case I posted a couple years ago (one of the most read posts of all time).  You can see that in leads V2, V5, and V6, as well as leads aVR and aVL, there is ST elevation. There is reciprocal ST depression in leads II, III, and aVF.

Case continued:

He had return of ventricular fibrillation immediately after the ECG was recorded (total time in regular rhythm was 2 minutes.)  LUCAS was restarted.  100 mg lidocaine was given.  Defibrillated again, no response.  100 mEq of bicarbonate, 40 U of vasopressin, 1 mg of epinephrine were given.  LUCAS was held briefly and there was wide complex pulseless electrical activity with no cardiac activity seen on ultrasound.  Then the patient reverted to V Fib again.  He was defibrillated again into sinus for only a few moments, then V Fib again.

At this point we realized we were dealing with incessant ventricular dysrhythmias, also known as "electrical storm," a condition seen almost exclusively during severe ischemia/STEMI.  We have had previous success with beta blockade using esmolol (which is short acting and can be turned off if it results in cardiogenic shock), so we gave 40 mg (500mcg/kg) of esmolol in a bolus, and started a 4 mg/min drip (50 mcg/kg/min).  We gave another 3 g of calcium, 1 mg of epinephrine, and 1 mg of atropine.

A venous blood gas returned: pH = 7.05/pCO2 = 101/pO2 = 25 (venous, remember)/HCO3 = 27.  A lactate returned at 12.8 mEq/L.  Another 50 mEq of bicarb was given.  The patient was defibrillated again after 38 minutes in the ED, and 68 minutes since his arrest.  He converted to sinus.  LUCAS was held.  Cardiac ultrasound showed function with poor ejection fraction.  Therapeutic hypothermia was started.

A repeat ECG was recorded while waiting for the cath team to arrive:
It appears to be a junctional rhythm at a rate of 55, with one PVC.  Now the anterolateral STEMI is clearly seen.  Interestingly, the ST elevation in V1-V3 is best seen in the PVC, with proportionally excessively discordant ST elevation (ST/S ratio V2 = 4/7 = 0.57, V3 = 4.5/14.5 = 0.31)

He was given aspirin and heparin and taken to the cath lab where a proximal LAD occlusion was opened.  A balloon pump was placed.

There were difficult critical care issues with  shock, low systemic vascular resistance and poor cardiac output, as well as pneumonia. Next day ejection fraction was 25% and peak troponin I was 250 ng/ml.

48 hours after arrest, he was awake and following commands. Within a few days, his wife could not tell any difference from his baseline functioning.  There was complete neurologic recovery.

His ejection fraction 3 months later is 40% and he is able to go 14 minutes on the Bruce protocol stress test (most normal people cannot even do that).  He will be back to work shortly.



Dr. Brian Driver, 4th year emergency medicine/internal medicine resident at Hennepin County Medical Center, gathered a 5-member panel to discuss: Cardiac Arrest: New Innovations and Best Practices.  

Panel members:

  • Dr. Brian Mahoney, HCMC EMS director and HCMC site investigator of the ResQTrial.  HCMC EMS has among the highest resuscitation rates in the country (2010 Utstein number, before use of LUCAS, = 49%, overall resuscitation success = 17%)
  • Dr. Demetris Yannopoulos, is an interventionalist at the University of Minnesota and is also a prolific cardiac arrest researcher at Minneapolis Medical Research Foundation (MMRF).  He and Dr. Keith Lurie do some amazing work in that laboratory.
  • Dr. Mark Sprenkle, of the Division of Pulmonary and Critical Care Medicine at HCMC
  • Dr. Gautam Shroff, staff Cardiologist, HCMC
  • Dr. Steve Smith of Dr. Smith's ECG Blog and staff emergency physician at HCMC

Dr. Driver wrote this concise summary of the panel discussion:



High-quality CPR is critical in cardiac arrest, and can increase the rates of successful
defibrillation and survival.(1) CPR should be performed with a compression depth of two inches at a rate of 100 per minute, allowing full chest recoil after each compression.

Ideal CPR can be difficult to maintain with manual chest compressions, and recent technologic advances have made it possible for devices such as the LUCAS to provide high-quality longlasting mechanical chest compressions at the proper rate and depth. Investigations are underway to determine the impact of the LUCAS on cardiac arrest survival.(2,3) Because high-quality CPR is known to improve outcomes, results are likely to be promising.

The impedance threshold device (ITD) is another new adjunct in cardiac arrest. This device
temporarily prevents airflow through the bag-valve mask or endotracheal tube during chest expansion (decompression phase of CPR), thereby augmenting negative intrathoracic pressure and increasing venous return and cardiac output. The ResQTrial, which compared standard CPR to a combination of active compression-decompression CPR coupled with an ITD improved survival in cardiac arrest from 6% to 9%.(4) Another trial using the ITD in pre-hospital cardiac arrest failed to show a benefit, but conclusions drawn from these data are limited because time to ITD placement was delayed.(5)  There is some data from this trial which was discussed and which further supports ITD use, but which cannot be published here, as it will be published in July 2013 and is embargoed at the moment.  The ITD should be used in conjunction with active compression-decompression CPR to fully realize the benefits of increased chest expansion with augmented negative intrathoracic pressure.

Hyperventilation is deadly: during cardiac arrest, it creates excessive positive intrathoracic pressure and decreases venous return and cardiac output. In an animal model, hyperventilation was associated with a decrease in coronary perfusion pressure and survival.(6) Patients in cardiac arrest should be ventilated at a rate of 10 breaths per minute.

Epinephrine, although featured in the ACLS cardiac arrest algorithm and used every day throughout the world, has never been shown to improve survival to hospital discharge. The benefits of epinephrine are currently limited only to increased rates of return of spontaneous circulation. Epinephrine is potentially harmful; in a recent large well-performed Japanese study pre-hospital epinephrine administration in cardiac arrest was associated with decreased survival and functional outcome at 1 month.(7) The best dose and time interval for epinephrine administration has not been defined, but because of these recent data it is prudent to minimize total epinephrine administered in cardiac arrest. Novel investigations into therapies such as nitroprusside that optimize blood flow instead of blood pressure are extremely promising, but have only been demonstrated in animal models.(8) (There are many more novel therapies being actively studied in the MMRF laboratory, especially by Drs. Yannopoulos and Lurie).  Our patient received 8 mg of epinephrine and survived.  How much did epinephrine contribute to his successful resuscitation, if at all?

In cases of refractory ventricular fibrillation or tachycardia, beta-blockade can result in less electrical instability.  One might worry that it would contribute to cardiogenic shock, but, paradoxically, it has the potential to improve inotropy by relaxing the semi-permanent state of left ventricular (LV) contraction and functional mitral stenosis induced by epinephrine.  It can thus improve LV filling and outflow. There are several case reports, as in this case, in which esmolol and other beta-blockers rapidly terminated refractory ventricular fibrillation and were associated with ROSC.(9,10) Certainly, administration of a beta-blocker should be strongly considered before terminating resuscitative efforts for a patient in incessant ventricular dysrhythmia. 

Additionally, there are a number of case reports in which even beta-blockade was ineffective, but in which a bedside left stellate ganglion block was performed and immediately terminated ventricular fibrillation.(11-13) A recent post detailing this procedure can be found here:

To the cath lab with ongoing chest compressions?  Finally, patients who arrest while in the ED and cannot be resuscitated may survive if transported with ongoing mechanical CPR to the cardiac catheterization lab for restoration of flow to an occluded coronary artery. During the panel discussion, the question arose as to whether percutaneous coronary intervention (PCI) is more easily completed without the motion artifact of chest compressions, and the utility of initiating extracorporeal membrane oxygenation (ECMO) to create ideal procedural conditions (14).  Dr. Yannopoulos, an interventional cardiologist and leading resuscitation researcher, stated that taking the time to place ECMO was not beneficial as PCI can readily be performed during chest compressions.  ECMO can be placed in the cardiac catheterization lab or in the ICU after the procedure, if indicated. PCI during mechanical CPR is probably only warranted when the time between arrest and intervention is extremely short.

Finally, all patients who are comatose due to cardiac arrest should undergo therapeutic hypothermia (this is so well established that it needs no elaboration).

Key Points:
• High-quality CPR is critical. Compressions should be 2” deep at a rate of 100 with full
chest recoil after each compression.
• Mechanical CPR can provide high-quality, long-lasting CPR.
• Active compression-decompression CPR with an ITD significantly increased survival in
cardiac arrest. These two adjuncts should always be used together to maximize benefit.
• Hyperventilation is fatal. Bag at a rate of 10 ventilations per minute.
• Epinephrine has no documented benefit of any clinical significance apart from ROSC,
and may be harmful. Total epinephrine dosing in cardiac arrest should be limited.
• Esmolol or other beta-blockers should be administered in refractory ventricular
fibrillation, and can lead to rapid ROSC. Ultrasound-guided left stellate ganglion blocks
are a last-line option for ventricular dysrhythmias that persist after all other therapies.

Use therapeutic hypothermia!

References
1. Wallace, S. K., Abella, B. S. & Becker, L. B. Quantifying the Effect of Cardiopulmonary Resuscitation Quality on Cardiac Arrest Outcome: A Systematic Review and Meta-Analysis. Circulation: Cardiovascular Quality and Outcomes 6, 148–156 (2013).
2. Rubertsson, S. et al. The study protocol for the LINC (LUCAS in cardiac arrest) study: a study comparing conventional adult out-of-hospital cardiopulmonary resuscitation with a concept with mechanical chest compressions and simultaneous defibrillation.
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 21, 5 (2013).
3. Perkins, G. D. et al. Prehospital randomised assessment of a mechanical compression device in cardiac arrest (PaRAMeDIC) trial protocol. Scandinavian Journal of Trauma,Resuscitation and Emergency Medicine 18, 58 (2010).
4. MD, P. T. P. A. et al. Standard cardiopulmonary resuscitation versus active compressiondecompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial. Lancet 377, 301–311 (2011).

5a. Aufderheide, T. P. et al.  Standard cardiopulmnary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial.  Lancet 2011;377(9762):301-11.

5b. Aufderheide, T. P. et al. A trial of an impedance threshold device in out-of-hospital cardiac arrest. N. Engl. J. Med. 365, 798–806 (2011).
6. Aufderheide, T. P. Hyperventilation-Induced Hypotension During Cardiopulmonary
Resuscitation. Circulation 109, 1960–1965 (2004).
7. Hagihara, A. et al. Prehospital epinephrine use and survival among patients with out-ofhospital cardiac arrest. JAMA 307, 1161–1168 (2012).
8. Yannopoulos, D. et al. Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest.  Critical Care Medicine 39, 1269–1274 (2011).
9. Miwa, Y. et al. Effects of Landiolol, an Ultra-Short-Acting β1-Selective Blocker, on Electrical Storm Refractory to Class III Antiarrhythmic Drugs. Circ J 74, 856–863 (2010).
10. Srivatsa, U. N., Ebrahimi, R., El-Bialy, A. & Wachsner, R. Y. Electrical Storm: Case Series and Review of Management. Journal of Cardiovascular Pharmacology and Therapeutics 8, 237–246 (2003).
11. Loyalka, P. et al. Left stellate ganglion block for continuous ventricular arrhythmias during percutaneous left ventricular assist device support. Tex Heart Inst J 38, 409–411 (2011).
12. Patel, R. A., Priore, D. L., Szeto, W. Y. & Slevin, K. A. Left stellate ganglion blockade for the management of drug-resistant electrical storm. Pain Med 12, 1196–1198 (2011).
13. Nademanee, K., Taylor, R., Bailey, W. E., Rieders, D. E. & Kosar, E. M. Treating Electrical Storm : Sympathetic Blockade Versus Advanced Cardiac Life Support-Guided Therapy.  Circulation 102, 742–747 (2000).
14. Kagawa E et al. Should we emergently revascularize occluded coronaries for cardiac arrest? Rapid-response extracorporeal membrane oxygenation and intra-arrest percutaneous coronary intervention. Circulation 2012 Sep 25; 126:1605.



24 comments:

  1. Wouldn't thrombolysis have been a last resort option considering the high probability that it's a STEMI?
    On the other hand, using a beta-blocker is certainly safer. That's one idea to remember.

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    1. Ana,

      This has been studied and was not effective: http://www.nejm.org/doi/pdf/10.1056/NEJMoa070570 (free full text)

      Steve Smith

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  2. I have a question about the "electrical storm". In the article you talk about using esmolol to treat the VF. Has any studies been done on using esmolol on someone that is having an electrical storm that manifests in VT instead of VF?

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    1. No, not that I know of. And the two are generally lumped together. Dr. Driver and I are going to do a retrospective on esmolol in cardiac arrest.

      VT is much more rare and hard to study.

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    2. PLEASE keep me posted with your findings. I find this hugely interesting - one of those things that makes too much sense to ignore.

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    3. A good overview paper was in Texas Heart Institute Journal, "The Evaluation and Management of Electrical Storm" by Eifling, Razavi, and Massumi. The literature they cite for B-blockers in cardiac arrest is mostly from the 90's and some from the 2000's, typically case reports of VF refractory to traditional therapies fixed with a B-blocker (propanalol, metoprolol, esmolol, etc).

      From "B-Blockers for the treatment of cardiac arrest from ventricular fibrillation?" in Resuscitation 2007 Dec;75(3):434-44.:

      "No human prospective randomized controlled trial has studied the effects of beta-blocker administration during VF directly. Prospective trials of anti-arrhythmics with beta-blocking properties have been published, as well as several case reports/case series and experimental animal studies. The evidence thus far suggests that beta-blockade during resuscitation from VF may be associated with increasing rates of resuscitation, greater post-resuscitation survival, and improved post-resuscitation myocardial function."

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    4. Thanks, Christopher.

      I also have this in my files:

      Use of beta-blockers for the treatment of cardiac arrest due to ventricular fibrillation/pulseless ventricular tachycardia: A systematic review; de Oliveira FC, Feitosa-Filho GS, Ritt LE; Resuscitation (Feb 2012). Resuscitation, Volume 83, Issue 6, June 2012, Pages 674–683.

      http://www.sciencedirect.com/science/article/pii/S0300957212000433

      Full text:

      http://emergencymedicine.pitt.edu/sites/default/files/Carvalho-2012-Use%20of%20beta%20blockers.pdf


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  3. Steve -

    Amazing case, and great discussion.

    - How fast do you give the esmolol bolus? I imagine that if I try this in the future, I'll likely be the one pushing it! Looking forward to the retrospective study.
    - Why the calcium and bicarb in this case? Of course, I realize that Dr Driver only had so much time for his discussion.

    Brooks

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    1. Brooks, sorry for late reply, found this one in my junk mail for some reason:
      Esmolol bolus can be given fast, just push. I was not the primary doc on the case, and my partner ordered the calcium and bicarb. I think he figured, why not? They were formerly on ACLS years ago and taken off. We were throwing in the kitchen sink. But it seems it was the esmolol that did it!
      Steve

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  4. Hello and what a great save. Way to think outside the box! Loving the esmolol... We're studing this in Cali also.

    My Question is regarding the depth of compressions. Since the ILCOR statements of depth are based on a average size person of 150lbs, why are there so many statements in this article saying you must push 2 inches, when we know so many should get more than that? Pushing 2 inches appears not to be the standard. "At least" 2 inches is. Pushing 2 inches on a 3 hundred pounder seems ineffective. This just bothers me. (I dont know the physical size of the pt, just for discussion)

    I would like some opinion.

    Jeff Laabs RCP

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    1. Jeff,

      Great question, and it took me so long to respond because I wanted to get the answer from the guy who knows more than anyone: Keith Lurie. He has great data on this that is embargoed right now, so you have to take his word for it. It will be published in July. There is also an abstract from Ian Stiell which I will reference below Keith's response.

      This is his response:

      Too little depth does not generate enough of an increase in intrathoracic pressure to propel blood forward. Too much depth cracks ribs, thus preventing good chest wall recoil which is essential for refilling the heart: it also increases the intrathoracic pressure too much so that the ICP increases to dangerous levels with each compression. A balanced approach is needed. 2” appears to be ideal based upon the ROC data for the total population . Even in obese patients 2” can be effective. The questioner is correct that it would be good to vary depth based upon body size, and chest compliance, and brittleness of ribs, and antero-postero diameter. Given that most cannot even get the rate and recoil right we do not know the importance of adjusting for weight or a large AP distance. Bottom line, 2” is enough for most patients since the pressures achieved in the thorax with that depth do propel blood forward. In the very obese pt we need to worry about pressure from the abdomen pushing against the diaphragm and the mechanics are pretty challenging at any depth…


      Ian Stiell et al. What Is The Optimal Chest Compression Depth During Out-of-hospital Cardiac Arrest Resuscitation of Adult Patients? Prehospital Emergency Care 2013;17:103.

      Results: For 9142 included adult patients, the mean compression depth was 41.9mm, with the following ranges: <38mm 37%, 38-51mm 45%, and >51mm 18%. The adjusted odds ratios for survival to discharge, with depth >51mm as reference, were <38mm, 0.69 (0.53, 0.90) and 38-51mm, 1.03 (0.81, 1.30). Covariate-adjusted spline curves revealed that the maximum survival was associated with a depth of 45.8mm, followed by a decline in survival by 50mm (optimal interval 44-49mm).

      Conclusions: This study found that more than one-third of patients received very low compression depth. The optimal CPR compression depth for survival appears to be 46mm but falls off after 50mm.

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  5. Khoi bui Minh
    Thanks, Dr Smith for a very interesting case. I learnt some critical points from this.
    I have some questions about drug administration when he was in ED. At that time, he was in VF, so why:
    - succinylcholin was used? I've never used muscle relaxants for cardiac arrest pt, it's not necessary, I think. Otherwise, it could produce some adverse effect
    -3g of calcium gluconate was given? It's not standard drug as AHA ACLS algorithm. And also administration of bicarb without bloodgas result, could these steps be done routinely?
    -10mins later in ED, why 2 miligram (not gram?) MgSO4 was given?
    Again, method of looking for STE as shown above reminds me of your previous post which made me very surprise and was very useful in many cases
    Thanks again

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    1. Good questions!

      1. Succinylcholine: his jaws were clenched and we could not intubate without paralysis
      2. We were trying anything. It had been 35 minutes. Years ago, calcium was recommended and later thrown out of the guidelines. We thought we had nothing to lose.
      3. Same answer with bicarb
      4. That was a typo, it is corrected now to grams

      Steve Smith

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  6. Amazing Dr.Smith!! Can Esmolol be used in VFib immediately does it have any efect converting to Sinus or its used only in "electrical storm" ?

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    1. I don't think there is enough data to know. But I would use it in refractory v fib or v tach, unresponsive to lidocaine and amiodarone.

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  7. I was just wondering what the rationale was for the 1mg of Atropine in what could be considered a tachydysrhythmia?

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    1. We had 3 of us doing the resuscitation and I was just advising, so that wasn't my order and I can't say for sure, but it might be good for brady arrhythmia and can't hurt.

      Delete
  8. Steve- GREAT case and SUPERB discussion - with most important this being a wonderful SAVE! So nice to have ready access to resuscitation guru Keith Lurie!

    I'm glad others asked about calcium - which I thought might have potential adverse effect - but you can't get a better end result than full recovery with normal neurologic function.

    I did want to comment on use of EPINEPRHRINE during cardiac arrest - about which I totally agree that Epi has never been shown to improve survival to hospital discharge. The optimal role of Epi (if any) in cardiac arrest is really unknown at this time. That said - to my reading, there are problems with the 2012 Hagihara study you reference (Ref 7) that I think question the contention that Epi is harmful.

    The trial was a non-randomized observational trial - so it isn't proof of cause-and-effect. Most patients did not receive bystander CPR - and 86-92% were in PEA/Asystole at the time EMS arrived - such that the cards were already stacked against potential for surival and improved neurologic outcome. Perhaps Epi did all that could be expected of it (ie, it increased chance for ROSC) - but given that most patients in the Hagihara study were already dead - increasing ROSC led to salvage of more "brain-dead" patients - ergo potential misinterpretation of results from this trial that "Epi was harmful" when the real conclusion to be drawn is that the chance for survival with intact neurologic status from out-of-hospital cardiac arrest with an initial mechanism of PEA/Asystole is extremely small ....

    Your great discussion clearly highlights the exciting new advances in resuscitation - and indeed the ultimate role of Epi may be far more limited than it was in the past. But to my reading - we do not yet have any firm evidence that Epi per se is harmful - but rather of a need to determine which patients in cardiac arrest should be given Epi. Increasing the chance of attaining ROSC may not be optimal goal in a patient without realisatic chance of survival. All of this is of course even more complicated given recent advances with therapeutic hypothermia and high-quality CPR that are changing the potential for salvage among patients who never would have survived with intact neurologic status in the past.

    THANKS so much for presenting this inspiring case with positive outcome!

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    1. All true, but the context matters: Epi has never been shown to be beneficial to outcomes. We only use it because we can get the immediate feedback of an increase in pulse and blood pressure and that feels good and right, but is it?

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    2. The context is that we do not yet know the answer. Until we do - we should: i) Continue to look for the answer; ii) Apply beneficial new interventions as they develop (ie, therapeutic hypothermia; advancements in CPR technique); and iii) Contemplate potential pros and cons of Epi (there are both!) when considering use of Epinephrine during cardiac arrest. Again - GREAT case and discussion!

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  9. Very good discussion of this case. Thank you so much for the time. I have a question/comment comming into this as a long time ACLS instructor, EMS educator, and proponent of Hgh Performance CPR.
    As was said by other commenters, I also have some heart burn over your contention on EPI. I originally wrote an extensive reply , but n the end only echoed the others above.
    I will add this:
    The study you mentioned (Hagihara, A. et al. Prehospital epinephrine use and survival among patients with out-of hospital cardiac arrest. JAMA 307, 1161–1168 (2012).) Regarding epinephrine was actually performed during 2005-2008, before the major push for high performance CPR (which was barely mentioned in 2005 but really pushed in 2010…but only has taken off since).
    As you mentioned , the use of the LUCAS II CPR device has an impact. So to does the “pit crew” approach to CPR, CPR monitoring devices, RESQ-POD, Hypothermia, and any number of different interventions that were not in as wide use in 2005, or even 2010 compared to today.

    This, more than the fact that the study subjects were in Asytole/PEO, may be critical.


    For that study to be truly informative, it should be recreated using current CPR practices and guidelines (wich have improved dramatically). If EPI continues to show decreased outcomes, then we will have to par down the why, what of increased morbidity and mortality.
    In a nutshell: us of EPI *THEN* and use of EPI **NOW** is not an apple to apple comparison by any means. Drawing conclusions based on that older study is like comparing the processing power of a commodore 64 to that of a modern tablet or smart phone. A faulty comparison may result in an inaccurate assumption) that Epi is a negative predictor of outcomes when it may be another factor altogether (i.e. poor CPR, lack of hypothermia, SIRS/ARDS/MODS, or other causes).

    Until that happens, at least in animal models, we cannot discount the 13% improvement in ROSC (which is the first step in recovery) .

    Respectfully submitted

    Steve

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    1. Steve,
      Thanks for your insightful comments!
      Steve Smith

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  10. Why does a proximal LAD or Left Main cause a RBBB?

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    1. Because the LAD is the blood supply to the right bundle.

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