Resuscitation: What the @$#! do we know?

Maybe you have been in EMS long enough to remember the good old days of the early 2000’s. I sometimes long for the days where we knew that epinephrine, fluids, airway management and antiarrhythmic medications were lifesaving interventions.

These days I have no idea if the interventions I  perform during resuscitation attempts are  the right thing or not. what the bleep to we know

Should we give epinephrine in cardiac arrest? I don’t know.
What is the optimal ventilation ratio in cardiac arrest? I don’t know.
Are mechanical CPR devices in cardiac arrest beneficial? I don’t know.
Is there a reason to use anti arrhythmic medications in cardiac arrest? I don’t know.

I have some ideas about what I think are the best practices out there and I can tell you what I think based upon how I interpret the data but that amounts to nothing more than an opinion.  Treating a patient in cardiac arrest has become a strange moral landscape for me where I am trying to follow protocols and do what I think is most correct for the patient. These do not always line up.

Epinephrine: We simply do not know if epi is helpful or harmful in an adult cardiac arrest. While epi does undoubtedly seem to increase the chance of ROSC in a patient with a cardiac arrest, (Jacobs 2011) the downside is epinephrine may decrease the chance of them being discharged with a CPC score of 1 or 2, which is what matters.

Available data points to at least two observational studies have demonstrated worse neurologic outcomes with epinephrine given to out of hospital cardiac arrests patients (Hagihara 2012 and Dumas 2013). But, then again, perhaps it is helpful to some and harmful to some or it might depend on when it is given and if given early it is helpful but if given later in an arrest it is harmful (Ewy 2104).

The AHA is equivocal on the use of epinephrine in cardiac arrests saying it may be reasonable to consider giving it every 3-5 minutes. What I find alarming is  that the evidence review section regarding the use of vasopressors in cardiac arrest in the AHA guidelines has a total of just 3 citations.

One of the three studies cited showed no benefit to epinephrine in cardiac arrest (Jacobs 2011) and the other two trials showed “conflicting results” ( 5.3.3.1 in the 2015 ECC guidelines). I am unsure how the AHA came to the conclusion that there were “conflicting results” as both studies showed no benefit to administering a standard epi regime in adult cardiac arrest. The Machida study showed no benefit to epinephrine administration and the Hagihara study showed “among patients with OHCA in Japan, use of prehospital epinephrine was significantly associated with increased chance of return of spontaneous circulation before hospital arrival but decreased chance of survival and good functional outcomes 1 month after the event.”

I am unsure how a total lack of efficacy or a correlation with worse outcomes is a “conflicting result.”  I am at a loss as to how they arrived at the conclusion it might be reasonable to give epinephrine every 3-5 minutes. I think giving a drug that may be harmful and lacks real proof of efficacy is unreasonable, at least with the current evidence available until 2019.

Mechanical CPR devices. This is another thing that at one point seemed like it might be a really good idea. I bought in to it hook, line and sinker.

It seems like in a controlled environment they are as good as anything once they are on the patient. However in real life it seems that something is different, for some reason patients who get mechanical CPR (mCPR) have worse outcomes than patients that received conventional CPR (cCPR).
In June 2016 a study of the Utah Cardiac Arrest Registry to Enhance Survival found Survival among Utstein victims –those with a witnessed arrest and an initial shockable rhythm –was 8/45 with (18%) with mCPR vs. 117/322 (36%) with cCPR (Youngquist). Certainly not a large enough sample size to throw the LUCAS device in the dumpster but at the same time this allows doubt to creep in.

A 2016 study drawing from the CARES registry found 5.6% of patients with mCPR had a good neurologic recovery vs 9.5%of the patients having cCPR having a good neurological recovery (Buckler, 2016).

Did we just waste $30,000 buying two LUCAS devices at my service? Is it the devices fault or is there an unaccounted for human factor such as improper placement of the device or a lack of vigilance about proper placement? Is it the delay in compression when applying the devices? One study showed a median time for the application of the LUCAS at 32.5 seconds (Yost) and another showed a median application time of 39 seconds (Lyon). Is that enough time to cause a worse outcome? It certainly seems possible. Is a 30+ second delay in compressions a death sentence for those patients that might be salvageable?

In my opinion we should change protocols to ensure that the LUCAS is only placed on the patient after several rounds of manual cpr until more information is known.
Ventilations in CPR: Speaking to the common, garden variety adult cardiac arrest, not arrests from hypoxic causes, do ventilations matter? Are they helpful or are they harmful? The AHA is again rather equivocal on the whole thing.  They don’t recommend passive oxygenation…unless you are doing it, then sure, go ahead. “We do not recommend the routine use of passive ventilation techniques during conventional CPR for adults. (Class IIb, LOE C-LD)However, in EMS systems that use bundles of care involving continuous chest compressions, the use of passive ventilation techniques may be considered as part of that bundle. (Class IIb, LOE C-LD)” 4.7.4.2

Also the AHA says you should do 30:2 (4.5.2) but if you want to skip ventilations all together for the first three rounds that is reasonable as well (3.9.2)

Assuming we properly ventilate patients with a BVM (we don’t) is it better than nothing? Is a BVM better than passive ventilation?

At least one study has shown a marked increase in neurologic outcomes with witnessed arrest using passive ventilations (Bobrow, 2009).

We have strong evidence that oxygen is harmful in pulsatile patients with myocardial infarction, is it a big leap to imagine that it is harmful in pulseless patients with myocardial infarction?(Nehme)

Could the fact that we suck at using a BVM be helping patients? Is it our inadequacy to get a good seal using a bvm and deliver a meaningful tidal volume to cardiac arrest patients in fact saving them by not over-ventilating them? Best answer to the question? I don’t know.

Amiodarone: I do the QA for my agency. I had to speak with someone once about not giving amiodarone in a cardiac arrest. I think I might have to apologize to that person at some point.

The 2016 ALPS study really put some doubt out there about if amiodarone does anything that actually matters in cardiac arrest ,the same goes for lidocaine.

“In conclusion, in this randomized trial, we found that overall neither amiodarone nor lidocaine resulted in a significantly higher rate of survival to hospital discharge or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia.” (Kudenchuk 2016)

The AHA has the following to say about giving anitarrythmics in cardiac arrest patients with VF and pulseless VT, “Whether optimized high-quality CPR and advances in post–cardiac arrest care will enable the increased rates of ROSC with ACLS medications to be translated into increased long-term survival remains to be determined.” (section 5.3).

Digging deeper in to the AHA actual guidelines reveals this statement:
“Refractory VF/pVT refers to VF or pVT that persists or recurs after 1 or more shocks. It is unlikely that an antiarrhythmic drug will itself pharmacologically convert VF/pVT to an organized perfusing rhythm. Rather, the principal objective of antiarrhythmic drug therapy in shock-refractory VF/pVT is to facilitate the restoration and maintenance of a spontaneous perfusing rhythm in concert with the shock termination of VF. Some antiarrhythmic drugs have been associated with increased rates of ROSC and hospital admission, but none have yet been proven to increase long-term survival or survival with good neurologic outcome.”

Please pay attention to the part I put in bold.

The hope is that by defibrillating and giving amiodarone we can stop the heart from being in the dysrhythmia and something better will appear. Sounds good so far, except for the fact that amiodarone decreases sinus node automaticity; it also slows conduction and increases refractoriness of the AV node. (Connolly 1999).

Again we find ourselves giving a drug without a single shred of evidence that we should use it, while using  it has at least a theoretically risk based on physiology.

I am tired of cringing every time I push the plunger. I am tired of the self-doubt that comes with the decision to perform apneic oxygenation or traditional ventilation. I am tired of giving medications that are almost certainly not going to help because everyone is too scared to stop giving them.

I miss the good old days where I was full of confidence. It is just that maybe the good old days weren’t so good for our patients.

Citations:

Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011;82(9):1138-43.


Hagihara A, Hasegawa M, Abe T, et al. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA. 2012;307:1161-1168.

Dumas F, Bougouin W, Geri G, et al. Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients? J Am Coll Cardiol. 2014;64:2360-2367.

Ewy GA. The time-sensitive role of vasopressors during resuscitation of ventricular fibrillation. J Am Coll Cardiol. 2014;64(22):2368-70.

Machida M, Miura S, Matsuo K, Ishikura H, Saku K. Effect of intravenous adrenaline before arrival at the hospital in out-of-hospital cardiac arrest. J Cardiol. 2012;60(6):503-7.

Buckler DG, Burke RV, Naim MY, et al. Association of Mechanical Cardiopulmonary Resuscitation Device Use With Cardiac Arrest Outcomes: A Population-Based Study Using the CARES Registry (Cardiac Arrest Registry to Enhance Survival). Circulation. 2016;134(25):2131-2133.

Youngquist ST, Ockerse P, Hartsell S, Stratford C, Taillac P. Mechanical chest compression devices are associated with poor neurological survival in a statewide registry: A propensity score analysis. Resuscitation. 2016;106:102-7.

Yost D, Phillips R, Gonzales L, et al. Assessment of CPR interruptions from transthoracic impedance during use of the LUCAS mechanical chest compression system. Resuscitation. 2012;83:961-965.

Lyon R, Crawford A, Crookston C, et al. The combined use of mechanical CPR and a carry sheet to maintain quality resuscitation in out-of-hospitalcardiac arrest patients during extrication and transport. Resuscitation. 2015 Aug;93:102-6.

Bobrow BJ, Ewy GA, Clark L, et al. Passive oxygen insufflation is superior to bag-valve-mask ventilation for witnessed ventricular fibrillation out-of-hospital cardiac arrest. Ann Emerg Med. 2009;

Nehme Z, Stub D, Bernard S, et al. Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction. Heart. 2016;102(6):444-51.54(5):656-662.e1

Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. N Engl J Med. 2016;374(18):1711-22.

Stuart J. Connolly. Evidence-Based Analysis of Amiodarone Efficacy and Safety. Circulation. 1999;100:2025-2034, originally published November 9, 1999

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4 thoughts on “Resuscitation: What the @$#! do we know?

  1. Ahhh, the good old days, when you couldn’t finish working a code unless you did escalating doses of Epi (1mg, 3mg, 5mg, repeat 5mg q5min until all the epi in the county was gone), maybe a few doses of Atropine, Bretylium, Lidocaine, Procainamide, Magnesium, and finish with a 2nd amp of Sodium Bicarb. The days when your ACLS instructors felt they weren’t doing their job right if half the class wasn’t crying by the time their Megacode was over.

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  2. Brian,

    I have come to a few realizations on this topic. Most important is that most guidelines are a numbers game. Most sudden cause of cardiac arrest, that witnessed outside of the hospital, is roughly 70% (depending on what study you like) caused by MI.

    Looking at inhospital arrest, the incidence of MI does not come close to that. Many patients simply experience the decompensation of another disease process which leads to cardiac arrest.

    While often equated, cardiac arrest is not a discreet pathology, it is a symptom of another pathology.

    I have come to understand disease processes over time. With different inciting factors and different time points, in different physiology based on physical development, compensation and decompensation follow a pattern. We define how fast this pattern is with “acute” or “chronic”, but it does not stipulate where in the process the patient is.

    The inciting cause and where in the process is crucial to first determining if resuscitation is possible. The end stage cahexic cancer patient is not resucitatable. That is a pretty clear case. But sometimes it is not so clear.

    This then leads to the action of organ support. Intubation, CPR, mechanical ventilation, etc. Organ support is rarely a treatment for the underlying pathology. Rescusitation as it is performed by non-intensive care experts is really not treatment or cure, but organ support.

    From there you must choose which organs you are supporting and how.

    Using epi as an example, in sudden cardiac arrest is there a lack of endogenous catecholamine? No. So why would administering one help? Is there an adverse effect of catecholamine OD? Yes. It inhibits circulation to multiple organs, not least of which are the brain and kidneys. Does that make it reasonable for immediate administration in bolus doses in SCA? No. Do the studies demonstrate that? Yes.

    Now compare that to a septic patient, who has both inhibition and inability to produce enough exogenous catecholamine for homeostasis. If this person arrests, would a catecholamine help? Yes. Do the studies show that? Yes. It is even reproducable in non-arrest situations like general anesthesia, which is about as close to arrest and treat with organ support as one can get.

    So what should you do in cardiac arrest? Well…It depends on what the cause was, what organs you need to support, and where in the compensation>decompensation>shock>MODS>MOF>death pathway you are based on underlying cause.

    Do you always know the underlying cause? No. So at that point, you must choose what organs you are supporting and how until you or somebody else has a reasonable idea or the patient dies.

    Is mechanical CPR better than high quality manual CPR? No. Studies support that. Is mechanical CPR better than low quality CPR? Yes. Can the 200lb solid muscle firefighter provide quality CPR on the hard flat ground? Yes. Can the 60 year old nurse provide quality CPR on the air mattress on a soft bed in the med surg ward? No.

    It seems to me that your conundrum is simply trying to find a simple one-size-fits-all solution to a very complex problem which is grossly oversimplified.

    You know a lot about resuscitation, the question is really, how do you apply what you know?

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  3. Great read, Brian. I’m not sure we’all ever have data that shows that anything is truly beneficial when applied to “sudden cardiac arrest” in general, without breaking it down into specific root causes. I think each of the AHA “suggestions”, formerly known as recommendations, probably has value in certain situations, but never when applied as a blanket treatment to SCA.

    I too miss the days of my naive false confidence that everything I did in a code was what was best for the patient.

    Also, my new favorite word is now refractoriness….thanks.

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  4. I have always wondered if all these studies and research take into consideration age and underlying medical problems?

    Back in the days when I was a Paramedic (1986-2001) things were very different than today, however my experience was that victims of sudden cardiac arrest without underlying medical conditions had a higher rate of recovery than people with known medical issues.

    I wonder if the AHA is mixing apples and oranges when doing their research and studies?

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