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Trouble with the NEW ACLS Guidelines

Discussion in 'ALS Discussion' started by arharris83, Nov 23, 2011.

  1. arharris83

    arharris83 Member

    Location:
    Lincoln Ne
    EMS Training:
    EMT-Paramedic
    I have been having trouble with the new ACLS guidelines because unfortunately I took ACLS literally 2 weeks before the new stuff came out. Any suggestions on how to decipher the new from the old?
  2. JPINFV

    JPINFV Gadfly

    Location:
    404: No Meme Found
    Are the big changes from an EMS standpoint basically:

    Don't use atropine for asystole.

    Don't give oxygen unless the patients with ACS unless they are hypoxic.

    Push hard, push fast.
  3. arharris83

    arharris83 Member

    Location:
    Lincoln Ne
    EMS Training:
    EMT-Paramedic
    Yesterday I was practicing Dynamic Cardiology for my NR Skills exam next week and I was told to learn the Hypothermic protocol for ROSC and I was like we haven't been told any of that during class which was done on the 17th. The instructor testing me out also said that Adenosine can be used in Vtach Stable as well as the normal PSVT. I was also told that you chose Amiodarone Infusion ORRRR Lidocaine with Vtach as well. Am I wrong to Cardiovert someone at 200J Biphasic when ACLS now says 120J's to start out?
  4. JPINFV

    JPINFV Gadfly

    Location:
    404: No Meme Found
    I don't remember off the top of my head what the current ACLS guidelines are for adenosine and amiodarone. In regards to the power setting for biphasic, I believe that hasn't changed from, "Use the manufacturer's recommended settings."
  5. usafmedic45

    usafmedic45 New Member

    Location:
    Indiana
    It depends on which protocol you are using. There are quite a few out there. Is there actually an AHA one now? It's been a while since I took ACLS and I hadn't heard mention of a ROSC therapeutic hypothermia protocol per se other than an endorsement of its use.
  6. tssemt2010

    tssemt2010 New Member

    1st dose amiodarone is 300, second is 150, then move onto lidocaine
    1st dose of adenosine is 6, then 12 and 12, max of 30

    its still use manufacturers recommendation on the biphasic monitor
  7. Cawolf86

    Cawolf86 New Member

    I believe he was referring to VT with pulses sicne he was comparing Adenosine and Amiodarone. In that case the initial dosing of Amiodarone would be 150mg over 10 minutes.
  8. WTEngel

    WTEngel New Member Premium Member

    Location:
    Ft. Worth, TX
    This is the official update article available from the AHA regarding the new ACLS changes, and the science behind them.

    My advice, do not ask people about the changes, as most are extremely uninformed, up to and including your instructors. Most ACLS instructors haven't even taken the time to read the Circulation Journal article regarding the updates. The link I am providing is the official word from AHA, and it is available for free online.

    http://circ.ahajournals.org/content/122/18_suppl_3/S729

    Click on the "free PDF" link on the right.

    Regarding what others have said in this thread already...

    Atropine has been removed from the Asystole/PEA protocol, even in the presence of a bradycardic PEA.

    SPO2 is to be titrated in ALL patients to between 94% and 99%. In other words, oxygen is only applied to patient who have SPO2 values <94%. Oxygen can be lowered or removed once 100% SPO2 has been achieved.

    Stable tachycardia can get 6 mg of adenosine initially, and then ONE follow up dose of 12 mg. There is no longer a recommendation for a third dose.

    Adenosine has been shown safe for treatment and diagnostic use in wide complex regular tachycardias, however should be avoided in patients with wide complex irregular or polymorphic tachycardias, as it has been shown to cause the rhythms to degenerate into VF.

    All UNSTABLE tachycardias, regardless of origin, get electrical cardioversion without delay. Do not attempt any other treatment unless cardioversion is absolutely not available.

    Synchronized cardioversion energy dosages are rhythm specific.
    -50-100 J biphasic for narrow complex regular tachycardia.
    -120-200 J biphasic (or 200 J monophasic) for narrow complex irregular tachycardia.
    -100 J for wide regular tachycardia.
    -120-200 J unsynchronized defibrillation dosage for all irregular wide complex tachycardias.

    As far as hypothermia protocol is concerned, AHA only recommends that it be initiated as early as possible post resuscitation in the victim who is unable to respond to verbal commands. They do not have a specific protocol, however mention that the current best practice is to lower the patient's body temperature to between 32 and 34 degrees celsius within 2-4 hours post resuscitation, and maintain that temperature for 24 to 48 hours. They recommend multiple methods, up to and including cold saline, air cooling devices, and circulated cold water devices, to name a few.

    I hope this helps. This is by far not a comprehensive list of changes, in fact it only scratches the surface. All of the changes and the scientific basis for the changes is available direct from the AHA at the link I provided above. They also post free images of the new algorithms.

    Like I mentioned earlier, take other people's advice with a grain of salt, unless they can produce the proof.
    Last edited by a moderator: Nov 23, 2011
  9. DrankTheKoolaid

    DrankTheKoolaid Active Member

    Location:
    NorCal
    re

    On the road atm but the incoming medical chairperson for the AHA did a recorded Q and A explaining the rational with all the changes. Quick google search should find it. Ill recheck post later if I ever make it back to the office.. My intern is a crap magnet......
  10. tssemt2010

    tssemt2010 New Member

    correct, pulsless vtac/vfib is 300mg initial dose, with pulses the dose is cut in half and spread out over 10 minutes
  11. jjesusfreak01

    jjesusfreak01 New Member

    Location:
    St. Georges, Grenada
    EMS Training:
    EMT-Intermediate
    We do hypothermia during cardiac arrest. Medical director says it is improving outcomes.
  12. IrightI

    IrightI New Member

    EMS Training:
    EMT-Paramedic
    Lido is not in the new ACLS guidelines. Some services however still have Lidocaine in there protocols. For pulseless V-tach/V-fib its 300 amio, 150 amio, then you can move to 40 units of vasopressin, followed with your 1mg epi for the remainder. AS stated before, for V-tach with a pulse or for a sinus rhythm with runs of v-tach you can hang 150 amio and give it over 10mins.

    Our service does have the protocol for hypothermic resuscitation. The new ACLS guidelines outline that as if you have ROSC and pt is still unresponisive you can hang 1-2L NS at about 84 degrees, followed by a drip of dob, levophed, whatever your service carries.

    I would only light someone up at 120J if its an irreg rhythm such as a-fib with rvr and my pt is unstable (i.e..hyptoensive, altered, shock, etc). A-fib does not repsond to any energy setting less than 120J, thus the new guidlines say to start at 120J. The only time im thinking about 200J is obvioulsy cardiac arrest, or torsades. SVT gets a start at 50, then works up to 200J if they cant convert at a lower setting.
  13. WTEngel

    WTEngel New Member Premium Member

    Location:
    Ft. Worth, TX
    Lidocaine absolutely is included in the new ACLS guidelines.

    Quoted from the AHA Circulation journal regarding 2010 updates to ACLS:

    "Lidocaine may be considered if amiodarone is not available (Class IIb, LOE B). The initial dose is 1 to 1.5 mg/kg IV. If VF/pulseless VT persists, additional doses of 0.5 to 0.75 mg/kg IV push may be administered at 5- to 10-minute intervals to a maximum dose of 3 mg/kg."

    It does say that amiodarone is associated with higher initial success than lidocaine, and ultimately amiodarone is the preferred first line antiarrhythmic, but to say it is not included in the guidelines is incorrect.

    Also, your listing for the drug sequence in pulseless VT/VF is confusing, and I am not sure if it is correct. The first med administered in the pulseless VT/VF algorithm is a vasopressor. At the next rhythm check, if the VF/VT persists, the patient is shocked, and then an antiarrhythmic is given, preferably amiodarone 300mg, or lidocaine at 1-1.5 mg/kg if amiodarone is unavailable. At the next rhythm check, assuming the rhythm is unchanged, another shock is administered, followed by a vasopressor again.

    Vasopressin may be used as the first or second vasopressor, but not for both, and should no longer be considered after the first two vasopressors have been given. Alternatively, epi may be given throughout the code from start to finish, and vasopressin may be completely excluded if the provider so chooses.

    Please show me where AHA recommends the information above. That may be YOUR service's protocol, but as far as I know, AHA has not outright recommended a method for cooling patients post arrest. They simply state that hypothermia therapy should be considered for appropriate patients as soon as possible after arrest, and recommend no particular method as being superior to the other, and certainly do not go so far as to recommend specific fluid temperatures.

    I see nowhere in the literature where it recommends going beyond 100J biphasic for SVT, unless specifically instructed to by the manufacturer of the device. The recommend STARTING at 200J monophasic for SVT, but that is a different story all together.

    Please be careful what you post. Some people here may take it as the gospel, and end up failing an evaluation.
  14. WTEngel

    WTEngel New Member Premium Member

    Location:
    Ft. Worth, TX
    Hypothermia DURING cardia arrest? Very interesting. I would like to see the research on that.

    The thing I find most fascinating about your comment is that hypothermia is listed specifically as one of the reversible causes of arrest, so it stands to reason that it should be avoided until ROSC is achieved.
  15. STXmedic

    STXmedic Forum Alchemist Premium Member

    Location:
    Texas
    EMS Training:
    EMT-Paramedic
    I've read at least one study on this that showed improved outcomes. Thought I had it saved... Might be a hard copy. I'll check for it.
  16. JPINFV

    JPINFV Gadfly

    Location:
    404: No Meme Found

    Thinking it through as a thought exercise (so don't ask for sources), I can see a difference between inducing hypothermia in a warm patient, and being concerned about hypothermia as a cause. How long does it take to dump a patient's temperature to therapeutic levels (I honestly don't know, hence the question). If it takes a while, I can see the benefit of being at a proper temperature when ROSC is achieved, instead of obtaining ROSC, and then lowering the temperature.
  17. WTEngel

    WTEngel New Member Premium Member

    Location:
    Ft. Worth, TX
    The current science recommends that a patient who is mildly hypothermic when ROSC is achieved should not be actively re-warmed, but does not recommend inducing hypothermia prior to achieving ROSC.

    The evidence around hypothermia therapy and the time period that it should be instituted is still being evaluated. While we do know that earlier tends to be better, the results were not all that dramatically different between patients who had hypothermia within minutes of ROSC vs. patients who had hypothermia initiated up to two hours later.

    With that in mind, while earlier initiation of hypothermia shows better neurological outcomes, if hypothermia during resuscitation reduces the chances of ROSC, does the potential neurological benefit exceed the potential risk of persistent arrest?

    Also, I wonder if the family of a patient who had hypothermia induced DURING resuscitation, and did not achieve ROSC, would have a platform for litigation? Hypothermia is a known reversible cause of pulseless arrest. Is inducing hypothermia during resuscitation possibly trading one cause of arrest (most likely ACS in the adult patient) for another (hypothermia)? Even though we could likely determine the initial etiology of arrest, would it be possible to reliably determine that it was the initial etiology and not the hypothermia that caused the arrest to persist?

    Just food for thought anyway...
  18. usafmedic45

    usafmedic45 New Member

    Location:
    Indiana
    As long as you keep them above 92-94 degrees F, you should be somewhat OK. Then you could drop them a little more once you get them back and stabilized.
  19. WTEngel

    WTEngel New Member Premium Member

    Location:
    Ft. Worth, TX
    In general I agree. A balanced approach is best.

    The patients who achieve ROSC are not the problem, it is the ones who do not. If you transferred a coding patient with a core temp of 92 to 95 F to the ER, how long would they work them before deciding to terminate? Would they terminate with a core temp that low? The questions are hypothetical of course, I know there are too many variables to give a general answer, but it is interesting to consider.

    I am not sure if there is any research available on the rate of ROSC in patients with non-hypothermic etiology, who have hypothermia induced while pulseless, compared to similar patients who do not have the hypothermia initiated until after ROSC. From what you guys are saying, it sounds like some areas are experimenting with it. I would definitely like to see some of the numbers.
  20. Handsome Robb

    Handsome Robb Youngin' Premium Member

    My undereducated opinion:

    In our litigious society, I'd bet that initiating therapeutic hypothermia during the arrest rather than post ROSC would give the lawyer something to stand on. I'd think their argument would be: "There are no studies to support this practice and it is not recognized as a 'standard of care'. "

    My understanding of therapeutic hypothermia, post ROSC , is to slow cellular metabolism which reduces the need for glucose and oxygen among other things to 'free up' these resources for the cells needing them to repair/replace tissue that was damaged during the arrest (very oversimplified). I may be way off base here, so by all means, please tell me if I'm wrong.

    My thought is if victims of a cold water drowning can survive *extremely* long "down"/submersion times with better success rates than that of the standard, non-hypothermic arrest since their metabolic demand is so low due to the slowing of cellular metabolism from the hypothermia. Why wouldn't minor to moderate therapeutic hypothermia be beneficial in all arrest that present in a viable or even a non-viable rhythm? I would think the decreased metabolic demand would increase the chances of ROSC and possibly survival-to-discharge unless the hypothermia would have a negative effect on the body's ability to deal with the metabolic acidosis from the arrest.

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