60 year old male CC: Sudden cardiac arrest

Here's a great case submitted by a faithful reader who wishes to remain anonymous. Some minor details have been changed to preserve patient confidentiality and some relevant comments and teaching points have been added.

EMS is called to a barbecue festival for 60 year old male, unconscious and unresponsive, possible cardiac arrest.

En route dispatch advises, "the caller states the patient is breathing, CPR in progress." 

While radio transmissions like this often make EMTs and paramedics chuckle, we know that agonal breathing helps predict survival from sudden cardiac arrest.

This is one of the reasons that "look, listen and feel" has been removed from the 2010 AHA ECC guidelines.

"Agonal gasps are common early after sudden cardiac arrest and can be confused with normal breathing. Pulse detection alone is often unreliable, even when performed by trained rescuers, and it may require additional time. Consequently, rescuers should start CPR immediately if the adult victim is unresponsive and not breathing or not breathing normally (ie, only gasping). The directive to "look, listen, and feel for breathing" to aid recognition is no longer recommended."

On arrival, bystander CPR is in progress. Specifically, continuous chest compressions without rescue breathing are in progress. An EMT takes over compressions and the following sequence happens very quickly.

  1. The LP12 is powered on.
  2. The combi-pads are deployed and attached to the patient.
  3. The LEAD button is pushed to get a paddles view.
  4. The monitor is charged to 200 J.

This is where the "pit crew" concept or "choreographed model" comes into play. There is no reason to hesitate. The monitor should be charged immediately with the expectation that it's a shockable rhythm so that the shock can be delivered as soon as possible.

(Since some are claiming this is "dangerous" please see:

M.S. Lloyd, B. Heeke, P.F. Walter, J.J. Langberg. Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 117 (2008) (2510 – 2514).

Edelson DP, Robertson-Dick BJ et al. Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study. Resuscitation. 2010 Nov;81(11):1521-6.)

Once these actions are complete, everyone clears the patient with the exception of the chest compression man. When the lead paramedic gives the command (in this case a nod of the head) the chest compression man clears the patient, the lead paramedic confirms that VF is on the monitor, and the shock is delivered with minimal delay between stopping compressions and shocking.

Compressions are resumed immediately. The pulse check does not occur until another complete 2 minute cycle is complete.

Incidentally, some of the highest performing EMS systems in the country handle this in differrent ways. Some perform continuous chest compressions with a non-rebreather mask, some follow the 30:2 recommendation of the AHA (occasionally with a ResQPOD attached to the BVM), others drop a blind insertion airway device like the King LTS-D and deliver asynchronous ventilations at a rate of 8-10/min. (every 6-8 seconds), and some capture the airway with a tracheal tube without interrupting chest compressions.

As the next 2-minute cycle is nearing completion the monitor should be charged again to 300 J (or whatever energy setting your protocols dictate for the second shock). Again, the idea is to avoid ineffficiency.

It shouldn't look like this:

  1. Stop compressions
  2. Read the monitor and decide the patient needs a shock
  3. Start compressions again
  4. Charge the monitor
  5. Stop compressions
  6. Confirm that a shockable rhythm is on the monitor
  7. Go through a lengthy "I'm clear, you're clear, we're all clear" process
  8. Deliver the shock

On the other hand, it is very important that the paramedic who interprets the monitor pay close attention to whether or not it's a shockable rhythm before pushing the SHOCK button.

This can be diffficult when the defibrillator is pre-charged, everyone's watching, and you're trying to balance minimizing the delay between stopping compressions and shocking with making sure the shock will confer a benefit to the patient.

After the second shock it was noted that the patient was "pinkening up."

The defibrillator was pre-charged prior to the end of the next 2 minute cycle. However, this time there was a rhythm on the monitor. It looked something like this.

The patient started to breath spontaneously at a rate of about 30/min which was somewhat surprising. The "airway man" attached the waveform capnography to the BVM and timed small bag squeezes with the patient's spontaneous ventilations. 

This works beautifully if you haven't tried it! Waveform capnography is a very useful tool.

Once the patient was loaded in the back of the ambulance a 12-lead ECG was captured.

Vital signs were assessed.

RR: 20
Pulse: 150 Irregular
NIBP: 155/123 (presumed spurious)
SpO2: 97 and rising

An EMT attempted to confirm the BP by auscultation but was only able to confirm a BP of 150/P.

At this point it was noted that the patient was moving and there was a small amount of vomit in the patient's mouth. 

The patient's airway was suctioned (with difficulty due to a clenched jaw). After a minute or two the patient's jaw relaxed.

The OPA was removed in case the problem was a return of the patient's airway reflexes. By this time the respiratory effort was adequate and the decision was made to switch the patient out to a non-rebreather mask. The patient's head was turned to the side.

This had a positive effect and within a minute or two the patient followed a command to open his eyes.

Another 12-lead ECG was captured.

By arrival at the hospital the patient was confused but talking.

Questions for discussion

Do you follow a "pit crew" concept or choreographed model for sudden cardiac arrest?

What is a normal response in your jurisdiction for sudden cardiac arrest?

Have you read the 2010 AHA ECC Guidelines?

Do you emphasize minimally interrupted chest compressions, controlled ventilations, and shocking in a 2-minute cycle?

Are all other interventions secondary?

Do you think this patient needed antiarrhythmics?

What do you think of the patient's 12-lead ECGs?

What should this patient's post-resuscitation care look like?

See also:

Conclusion to 60 year old male CC: Sudden cardiac arrest

High performance CPR – Seattle Style!

Sudden Cardiac Arrest podcasts from EMS Today 2011


  • Matt says:

    Great case to review.  

  • John P says:

    what was the etco2 value and waveform?

  • Nick Adams says:

    Nice, uncomplicated, scenerio. It reads as if everyone worked as a team and the lead Paramedic organized everything well. This is the key to getting a ROSC. I had a case just like this, but the patient did not wake up so easily. Prior to us arriving on scene, the patient was defibrillated by an AED, and was now in PEA. With a little oxygenation and ventillation, his pulse returned. 12 lead EKG showed a 2:1 HB with a wide QRS and RsR' in lead II (multiple HB's). With this, I decided to hold off on an antidysrhythmic. Otherwise I would have. If the patient was defibrillated with the LP or an AED, the patient was in a lethal dysrhythmia, requiring an antidysrhythmic. In this patient, I would start an Amiodarone bolus of 150mg over 10 minutes, followed by a maintainence drip. Because the patient woke up within a few minutes, and began to follow comands, I would not begin hypothermic treatment. 2 large bore IV's, O2 appropriate to need, continue serial 12 leads (the patient showed ST segment changes in his inferolateral wall within 6 minutes), ASA if the patient is now able to.  All while rapid deisel bolusing it to a hospital with interventional cath capabilities.

  • Christopher says:

    Not so certain about the second defibrillation, could be PEA or that could be some odd artifact. Regardless, well run code!
    First 12-Lead looks like ST w/ frequent PACs (epi on board?) with elevation in aVR/V1-V4 w/ reciprocal changes inferiorly. Second 12-Lead also looks like ST w/ frequent PACs, elevation remains in aVR but the remainder of the leads have marked changes in their ST segments (ST depression inferiolaterally and some in V4). Severe 3-vessel disease perhaps with the changes due to reperfusion? This isn't surprising in light of the gentleman's resuscitation from cardiac arrest. I'd give a heads up to the receiving facility and find out if they wanted to activate based on post-ROSC 12-Lead.
    Again, great job on the code.

  • Ryan says:

    I'm currently in my paramedic internship.  Question: with acute MI suspected and confirmed ST elevation, after ROSC and by the time this patient came around and was talking but "confused", would you start treating with STEMI protocol and give NTG?

  • VinceD says:

    I agree with Christopher that the second shock was not necessary, but in this case it didn't cause any harm and I don't fault the crew one bit for attempting to shock as quickly as possible; it's just a learning opportunity to take a deep breath while analyzing the rhythm. I also agree wih your analysis of the ST-changes between the two strips, however I'm seeing a-fib in both tracings. In the right precordials I see what could be a couple of p-waves, but the rhythm is very irregular and I'm not convinced they're legit. From Tom's rundown of the case, things were done amazingly well and this is a wonderful example of the right way to handle a code. Thanks for the awesome post!
    Hmm I'm not sure if I would give an antiarrhythmic. I'm pretty well convinced it's a-fib, and 150 bpm is a bit fast for my (and likely the patient's) liking, but he's also just returned from being DEAD, so I can't blame his heart for being a bit irritable. Although cardizem is my usual go-to drug for rapid a-fib, in this case if I were to give something, I would request amiodarone via med control (150mg over 10 minutes) since it would both provide rate control and theoretically help stave off some of the lethal arrhythmias. That being said, he is improving very rapidly at this point and has a respectable palpated BP, so unless I had a lengthy transport ahead of me, I'd more than likely leave well-enough alone on the rhythm front and see if things settle down on their own.
    Post-resus care on this patient would be mostly supportive in this patient as he seems to be doing most of the work himself. I agree with EMS's management of the airway thus far, but I would tell my airway person to keep following the airway and breathing with the Yankauer in hand; I don't want our uplifting CPR save dying from an aspiration pneumonia a week from now. No pressors and no hypothermia. I've seen good things about post-arrest PCI, and although I'm not sold on any particular lesion based on the two 12-lead ECG's (w/ resolving anterior elevation but maybe worsening inferolateral depression, it's a tough read with baseline sway), the patient would likely benefit from a coronary angio and I'd be heading to the cath-capable facility and seeing what they would like to do.
    I've rambled enough as it is so I won't share what's actually done in my region, but it's easy to say that most codes are not run like this one, although things are improving.

  • Christopher says:

    I'm paraphrasing Rogue Medic and a few of my mentors when I say this (and don't take it the wrong way, said Tongue-in-Cheek), "why mess with a good thing?" I think the only time I'd consider SL NTG post-resuscitation would be if I witnessed the arrest, responded with 1 shock, and after 15-20 minutes of a long transport, still had chest pain.
    The latest ACLS guidelines spend more time on post-ROSC care, but it still isn't adequate enough I think. Like you, I still have lingering questions!

  • Nick Adams says:

    OMG!!  I seemed to have missed the strip with the second shock.  I came back on this site to read what others thought and saw the comments about not shocking the second time.  OOPS.  My guess is that the patient was in VF just prior to the shock so the medic charged.  By the time the defibrillator charged, the patients rhythm may have spontaneously converted just before shocking.  It shouldn't happen, but it does.  Make sure you are looking at the rhythm just before you press the shock button.
    Anyway, I would also like to point out that the patient was in VF at some point, so an antidysrhythmic is indicated.  In order for a patient to go into a VF, thier venticles had to have been irritable at some point in time.  An antidysrhythmic may take care of this, so the verntricles doesn't do this again.  If the patient goes into VF "one more time"…….it may be the last time the Paramedic ever sees a perfusing rhythm.  So yes, an antidysrhythmic IS indicated (of course after an acceptable ventricular rate is acheived with no bi of trifascicular blocks).
    I would say with confidence that the ST segment elevation in aVR is a strong indicator of an LAD occlusion.

  • Christopher says:

    Well said. I should have paid more attention to the R-R in the limb leads. I saw "p-waves" and grouping in the precordials. I think you have me convinced it is AF.

  • BadgerMedic says:

    As always, I am really intrigued with the comments. In this post, one of the biggest points that I see, as my service is moving toward (officially) the "Pit-Crew" method, is the waisted time in the defib part of the code. It's something that even though stopping of CPR is hopefully minimized, can still be improved on.  Describing the defib sequence like the post did really brings to light how much time an un-organized code can waste – in areas where you might not expect it. Smoothing out the transition from CPR to rhythm check/defib is crucial and can sometimes be challenging when dealing with changing from the FD/First Responder's AED to the LP. Once again, thanks for bringing another example where the post and comments have made me think and see things that I might have otherwise overlooked. Please keep them coming!

  • VinceD says:

    Eh it's one of the benefits of not being the first to comment Christopher.

    Nick, I'm no expert on the matter, but in a case like this I'd be a bit wary of using aVR to try and identify the occlusion. In the first 12-lead, there is indeed elevation in aVR, but the depression is pretty well confined to the inferior leads and there is also clear elevation all across the anterior precordials. The sign you are alluding to requires extensive ST-depression across I, II, III, aVF, and V3-6 with elevation in aVR (with more specifity if aVL and V1 also have elevation), so this tracing doesn't fit the criteria. I'll agree that the second 12-lead does indeed resemble that description, but the rate is also 150 bpm in rapid a-fib after a cardiac arrest, so the pattern could very well be due to demand ischemia.

    Based on the history of cardiac arrest and transient anterior precordial elevation, I agree that there could very well be an LAD occlusion and I think you're on the right track, but I just wouldn't be using aVR to support my reasoning. On it's own that lead doesn't offer any specifity and it's my understanding that any time you have depression in I and II (or sometimes just either of those leads), you'll have elevation in aVR. It's only when you look at the entire ECG that the sign has utility. My understanding of this phenomenon is far from definitive, but maybe someone else out there can lend more weight to what is going on.

  • VinceD says:

    (sorry to take over the comments, too much free time on my evening off)
    BadgerMedic: Good point, and that is the area where I think the studies in "hands-on" defibrillation will be of great utility (defibrillation while the compressor still has their hands on the patient's chest, for those who aren't complete dorks that spend their free time reading research). I don't know how vital it will be for us to eventually shock patients while simultaneously performing compressions, but I think it will assuredly save time and avoid confusion if the compressor doesn't have to stop and back away from the patient while the shock is occurring. They will simply pause for a few seconds with theirs hands still on the patient's chest while the rhythm is analyzed and the shock is delivered, and then resume compressions the moment after the patient is shocked. That's the dream anyway.

    PLUS (I just realized) if you're using anterior-posterior pad placement, the compressor could apply pressure to the anterior pad, decresing the impedance and theoretically increasing the effectiveness of defibrillation. Now I'm not suggesting any of us actually go out and try any of this just yet, but one of these days it could be standard practice…

  • Dave B says:

    I agree with AF and many of the comments so far…
    couple of points.. as been reviewed here and elsewhere, those most in the know believe that elevation in aVR does not indicate occlusion, but rather severe disease… occlusion of the LMCA is incompatible with life… rather signifies severe multi-vessel disease, or collateral circulation… Chime in  Christopher??
    also, at my agency we have been transitioning and training with the "pit-crew" concept, and most importantly minimizing time off the chest… Compression Fraction has become the measuring tool of the day, where less time off chest directly correlates with higher survival rates… now… the law of unintended consequences… i can tell you that the issue of inappropriate shocks is real… we have already run into this.. it is not an issue of "taking a breath" before shocking, although that might be helpful… but rather the context of pushing that button has changed… there is now a different pressure to not waste time, and those complexes are flying by the monitor screen very quickly, all the while trying to stay "choreographed" and shock as soon as possible… the complexes are not always clear, and things change fast…i can tell you that while sitting down with a medic and reviewing a code, the complexes sure seem to look different on paper than they do in real time.  IMHO, this issue is not going away so quickly. Perhaps "no harm-no foul" this time, but will that always be the case?

  • Shalom says:

    Great case!
    With regard to the above ecg, I've heard many times that with tachycardias you cant truly diagnose STEMI because of the demand ischemia.
    Can demand ischemia cause STE or just STD?
    Is the STD of demand ischemia localized or can it appear in any leads?

  • Nick Adams says:

    VinceD,  Ok buddy, if you don't believe me, maybe you'll believe the Journel of the American College of Cardiology (JACC).
    aVR should never be elevated.  It is a sign of severe myocarial disease. 
    Rate induced ischemia (positive stress test?..lol) is a possiblility if there was no elevation in aVR.  Because there is elevation in aVR, I would conclude that this is due to a LMCA occlusion.  Especially if the elevation in aVR is greater then in V1.  Granted, an occlusion of the LMCA is not compatible with life…..the patient was dead at one point in this scenerio, but the occlusion can be partial, and/or with collateral circulation.  Another possibility is multi-vessel occlusion to include a proximal LAD.
    But I'm no expert either.
    Nick Adams

  • Christopher says:


    Dr. Smith cautions that ST-depression does not localize. So if you have ST-depression you are either seeing a reciprocal change or diffuse non-localizable ischemia.

  • Nick Adams says:

    I'm not localizing based on ST depression.  I'm localizing based on ST elevation in aVR.

  • Axel Foley says:

    I believe Christopher wasn't talking to you, Nick.
    Just wanted to say how interesting all these case-studies and most comments are and that I learn a lot just by reading this blog.
    Congratulations Tom and keep up the good work! I really appreciate it!

  • VinceD says:

    Dave B, good point on the use of the term "LMCA disease" since it's a different beast from the typical 99% or 100% "occlusions" that we worry about in STEMI's.
    Sorry in advance for the length (that's what he said)…
    Nick, I think I undersold my point and didn't explain it well enough. I used to have a big interest in aVR as a marker of LMCA/triple-vessel/proximal LAD disease after listening to a bunch of lectures from Dr. Amal Mattu, and had indeed read that editorial in addition to the studies it cites and whatever else I could get my hands on. Before diving into the literature I've even used it to disagree with a doctor's decision and been right, but now I think I was mostly lucky. He's a very smart man and it's possible he knows something I don't, but I have the feeling that he tends to oversell the utility of ST-elevation in aVR because of the climate where he practices and the need to overstate and oversimplify things to make a point while lecturing. He's not wrong to, it drives home a very important point, but it's something to keep in mind.
    Most of the studies that look at elevation in aVR do so in (small) populations of patients with confirmed ACS going to the cath lab in a non-emergent fashion. These are not our undifferentiated patients coming in with chest pain where we are trying to decide whether to activate the cath lab and clear a table. These were patients in whom the diagnosis of heart disease was pretty well established but their presentation did not warrant emergent revascularization. In such cases it is well proven that ST-elevation in aVR carries a much higher 30-day mortality and likelihood of needing CABG, and therefore should not be ignored. It does not, however, show that it is in any way a STEMI equivalent in that there is a morbiditiy or mortality benefit in getting the patient to cath in 60 minutes versus 120 minutes. Now if a region or hospital does want to make it a STEMI equivalent in protocols, then they certainly have the right and I see no fault in their commitment to expedite care, but it's far from a cut-and-dry decision and someplace that wants to wait several hours or even overnight in a stable patient is just as well reasoned.
    What these studies do not look at are patients who are hypoxic, tachycardic, or unstable, which are the cases that really cause us worry. STE in aVR is merely a marker of global ischemia and will arise whenever there is depression in both leads I and II. That is why it is associated with left-main, triple vessel, and proximal LAD disease. If blood flow is reduced through one of those three means, most of the heart will becomes ischemic, resulting in widespread ST-depression. Simply being hypoxic could have a similar effect on the heart, as could demand ischemia from tachycardias. Next time you have a person in SVT or very rapid a-fib where there are secondary ST-changes (usually widespread depression), take a look at aVR and it will be elevated. As soon as their rate is controlled the ST-segments will resolve, and it doesn't mean they need PCI or bypass.
    Making a hugely unwarranted jump and putting myself in the shoes of an ED physician, a sign like STE in aVR is important for two reasons. First, it can affect whether you want to give clopidogrel to a patient with ACS. Most of the time it's likely beneficial to give, but if the patient will require bypass, something you wouldn't know until cath, the CT surgeon may not want to touch them with Plavix on board, delaying intervention. There's one study out there that suggest a pretty good negative predictive value if there is no elevation in aVR (like 98%), so if that was the case you'd feel pretty safe giving them clopidogrel in the ED. Otherwise you'd leave the decision to the cardiologist. The second scenario would be to try and push through a case you feel needs cardiac intervention but your cardiology consult is reluctant. It may be Friday evening and the patient comes in for intermittent chest pain for a week or two with ST-depression throughout and elevation in aVR. The cardiologist may opine that it doesn't warrant emergent or urgent intervention and patient will be managed medically until Monday morning. The ED physician, knowing the poor prognosis of LMCA/triple-vessel disease over time (usually 30-day endpoints in the studies), can cite the studies demonstrating the badness of elevation in aVR and push the cardiologist to do something sooner, rather than waiting three days. I suppose it would also be of utility of the patient was unstable and needed immediate intervention and cardiology was stalling, but I haven't seen much pushback in scenarios like that in my experience and most cardiologist I've worked with will take them to cath to see what the deal is.
    In this case, the patient is clearly unstable and will need a cath on an emergent basis. In my opinion the reason for needing the cath is simply the fact that he arrested and supporting the decision are dynamic ST-changes, but I just don't see a strong enough case to try and call a culprit artery. I'm not very knowledgeable when it comes to how ST and T-waves will change over time in response to various ischemic states (Dr. Smith is the go-to guy for that), but with the combination of prolonged hypoxia from the arrest state, two defibrillations, possibly ACLS drugs, and rapid a-fib, there's a whole host of things that could be causing the changes we see. As I said before, yes I agree there's a good chance there's LAD/LMCA/triple vessel disease based on the fact that he died for a bit, there was transient elevation in the anterior leads, and there's now global depression, but I just wouldn't hang my hat on aVR to give me that answer.
    I apologize again for the superlong response, I don't think there's a simple explanation for this one and could go on for two or three more posts like this, but luckily for everyone still reading I won't…

  • Robert Piparo says:

    Cheers everyone… this is my first time posting to this site. I like the discussion boards here… They seem very educational.
    So here's my 3 cents on this call and as it would be handled in my system (County wide ALS ambulance response). 
    This call seems to be a strait forward VF arrest with an excellent key component. Bystander chest compressions!  The VF treated with a countershock as noted and appered to convert into a sub SA node rhythm  (looks IVR to me).  I don't think the 2nd shock was indicated.  As far as the post arrest Rx. The inital 12 lead appears to show a Anterioseptal wall MI (noted acute ST changes) in an AF (Noted by the R to R interval. Thinking LAD / LCA involement).  At this point I would like to establish V/S.  Also due to the nature of this call I think an Amiodarone bolus over 10 mins would be needed to reduce myocardial irritability and also my bring down that heart rate.  I think the Idea of using EtCO2 for ROSC is a gold standard  I think maintaining the 35 – 45 mmHg is very important due to the side effects of acute acidosis. IF he is not "blowing off" the CO2 as needed we need to correct this for him and be ready to assit and consider ETI.  Furthermore If the mental status does not improve to a GCS  > then 8 use of thereaputic hypothemia would be indicated.  Transmit 12 lead get to PCI center.
    Great forum! I look forward to learning more with all of you.

  • Axel Foley says:

    @ Tom: If I got it right, you are promoting a "CPR-choreography" in which the defibrillator is charged before analyzing the rhythm. Is this method just your personal interpretation of "defibrillation as soon as possible" or do the AHA-guidelines also recommend it?
    I'm curious to learn more about how you guys in the US handle things. Here in Europe, according to the 2010 ERC-guidelines, the sequence is: compressions > rhythm analysis > compressions while charging > shock.
    This method delays the defibrillation by a few seconds, because you charge after analyzing the rhythm, but the pre-shock pause is significantly shorter. (given a well trained team-approach)
    Is there any clear advantage of your approach that I don't recognize?
    And to all the other readers: Do you handle manual defibrillation the way Tom does?
    Sorry to ask all this, but I hope to learn more about your take on this topic and hopefully can take away some useful tips for my next cardiac arrest patient.

  • Cannulator says:

    I’m disappointed withe pit crew concept. I would snot someone waving a loaded weapon around me and would do the same with a charged defibrillator ‘in anticipation’ be leavied the same way.

    I have worked a system with a venue with an at times 84% survival from primary VF/VT many of them with SAEDS and lay responders without such a dangerous practice.

    Clear/ all clear and similar safety practices come before any dick swinging saves.

    I’m getting used to the ongoing assault of lay person primary life support every couple years so the removal if look listen and feel will grow on me I guess.

    In the end I defibrillate because I’ve assessed the patient needs it. Not because the AHA says we have to across the Pacific.

  • Except that a charged biphasic defibrillator isn't particularly dangerous.

    M.S. Lloyd, B. Heeke, P.F. Walter, J.J. Langberg. Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 117 (2008) (2510 – 2514)

    It's certainly not like waving a weapon around. This is mythology that originates with the fact that "I'm clear, you're clear, we're all clear" has been beaten into our heads.

    Let's deal in facts. How is precharging the defibrillator dangerous?

  • Cannulator says:

    It only takes one sly hand and it's now a discharged defibrillator. Especially if we get rid of I'm clear, you're clear, we're all clear.
    It's also worth noting that after the reply from a Physio Control scientist that the authors don't actually advocate compression during defibrillation or changing of the guidlines without further study. Despite this the Editor of the edition is so very quick to jump on the bandwagon and ask for a change to guidlines!!!

    Should our findings be interpreted as the "go-ahead" to ignore guidelines and perform compressions while shocks are delivered? Obviously, they should not. As pointed out in the Discussion, we do not advocate that this maneuver be used clinically until proven safe by further testing.

    If I am dealing in facts, who wears polyethylene gloves to a cardiac arrest? I wear latex or Nitrile.

  • Old Timer says:

    Ya'll need to relax on the 12-leads post ROSC. You can't trust anything except if you see an MI in there for at least 20 mins or so of settling down. Cells were just about at apoptysis here. Amazing work. Bolus with some calming medicine for the pissed off ventricles and hope that this is not the 25% range of v-fib that is clot in origin. 

  • Axel Foley says:

    I wasn't suggesting that precharging is dangerous.
    I was just wondering if there is any evidence (AHA?) that this method is more effective or does have any clear advantages that I overlooked so far. Because again, the ERC does not recommend this strategy.

  • VinceD says:

    Axel, I'm sure I'm not as familiar with all of the resuscitation literature as Tom and cannot speak for him, but here's what I see going on:

    One of the key determinants of a good cardiac arrest outcome is performing a lot of good compressions, which makes intuitive sense. What ends up being less clear, however, is just how those compressions create their positive impact. One of the things that I didn't realize when I performed my first CPRs is that when we press on the chest, we're not actually squeezing the heart to create a manual heartbeat (ala internal compressions during a thoracotomy). Most of what we're doing is modulating the intrathoracic pressure, which in turn increases the mean blood pressure of the aorta and coronary arteries stemming off of it (coronary perfusion pressure, CPP), one of the major determinants of whether someone will be successfully defibrillated. This increase in CPP doesn't happen the instant you compress the chest, however. It takes several compressions to build up a useful pressure, and as soon as you pause you lose everything you built up and have to start from scratch. That's one of the reasons we switched from a 15:2 to a 30:2 compression to ventilation ratio in adults. With the 15:2 ratio, as soon as you built up some coronary perfusion it was time to stop and give breaths again, but now with less pauses more time can be spent at that ideal level of CPP and not stopped or trying to build the pressure back up.

    So with that in mind, Tom's advocacy of charging the defibrillator before analyzing the rhythm eliminates the time where providers would do nothing while waiting for the machine to charge. Essentially it's the same thing the ERC recommends by having providers resume compressions again after analysis. This brings up the only possible disadvantage I see with the Europen method in comparison to what Tom is promoting: With his tweaks of the AHA protocol a greater percentage of compressions are being performed while maintaining a maximim CPP. With the European technique, while analyzing, you lose that ideal CPP that has been built up and spend time working the pressure back up when it's time to stop again and shock.

    IMPORTANTLY, that is merely an inference based on lab data in animal studies; in real life I'm fairly confident both methods are probably equally as effective when it comes to actual patient outcomes and I wouldn't suggest that one is superior to another. People could just as effectively argue in the opposite direction that by building the coronary perfusion pressure back up to an ideal level in the moments just before shocking, it may increase the effectiveness of the defibrillation by increasing the proximity of the shock to the last compressions.

    I hope that helped explained a very small part of the physiology going on here and where our rationale is coming from (Tom, correct me if you think of it differently). In my mind I've got diagrams I could draw out breaking down the time spent on various aspects of a cardiac arrest and their effect on coronary artery perfusion, but unless anyone actually wants to see them I think it's simply enough that as long as we maximize our time spent providing good CPR and minimize the interruptions (which both the AHA and ARC agree upon), we will be doing right by our patients.

  • But then, I'm not advocating that we defibrillate while our partner is performing chest compresssions. I'm arguing that the risk of pre-charging the defibrillator (so that it's ready to shock) is minimal and will prove to be therapeutic by both 1.) increasing the CPR fraction time and 2.) minimizing the delay between stopping compressions and shocking. Cops carry a round in the chamber and somehow they're able to make it through the shift without accidentally discharging thier weapon. The idea that someone is going to accidentally press the shock button a bit far-fetched, IMHO, especially when the "monitor man" is the team leader. Even if you concede that there is a higher risk of an accidental discharge of the monitor (which I disagree with) I'd like to see the evidence that it's dangerous.

  • Here's a study that looked at charging the defib during compressions.

    Edelson DP, Robertson-Dick BJ et al., Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study. Resuscitation. 2010 Nov;81(11):1521-6.

    Abstract here: http://www.ncbi.nlm.nih.gov/pubmed/20807672

    CONCLUSIONS: Charging during compressions is underutilized in clinical practice. The technique is associated with decreased hands-off time preceding defibrillation, with minimal risk to patients or rescuers. 

  • VinceD – I hope we can all agree that we should be performing compressions while the defib is charging and minimize the interval between stopping compressions and shocking. I think pre-charging the defibrillator will emerge as a best practice and experience will show that it's safe and effective. In the meantime, it's not worth arguing over if it distracts from the underlying principle. For myself, I will continue to emulate those EMS systems that demonstrate the highest save rates. I suspect my views will continue to evolve as we continue to zero in on the constellation of techniques and therapies that maximize neurologically intact survival from sudden cardiac arrest.

  • blake says:

    So I’m a paramedic student and reviewing the two 12’s I did not notice any viewable p waves and the rhythm is irregular with a wide qrs, I assumed accerlated junctional?

  • Joel says:

    Great case.  The part where it said the pt had the OPA removed and placed on an NRB, this having a positive effect.  Previously stated the SpO2 was 97% and rising.  According to the new AHA guidelines, titrating oxygen for SpO2 of 94% would have cause me to withold the NRB, and see how the pt would of fared on RA, then NC if necessary.  I wonder if the same outcome of the pt opening his eyes and beginning to talk would have happened without the high flow O2… as the AHA recomends…

  • Great case but it stopped short. It should continue. The patient was transferred to an experienced PCI center. Focused medical evaluation was performed in the ED and emergent cardiology consultation was obtained. Although there is not clear ST elevation on the 12 lead the interventional cardiologist knows the data that over 70% of VF cardiac arrests are caused by an acute coronary syndrome. The decision is made to take the patient for emergent cardiac cath because the highest risk for death after a cardiac arrest is in the first 24 hours. Access is gained via the radial artery and an occluded (take your pick; LAD, circ or RCA) is found. PCI is performed. The patient is discharged 3 days later with normal LVSF and will follow up in cardiac rehab in 2 weeks. Obviously, we are continuing with the best case scenario that this case exhibits.

    FYI: there was a comment that LM occlusion is not compatible with life and this is false. I think the overwhelming majority of the time that is true but I have scented an acutely occluded LM wondering the entire time why the patient was alive. He made it.

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