2010 AHA Updates

It's that time again.  As most of us Americans in the wide world of emergency medicine know, every five years the American Heart Association updates their recommendations.  Those recommendations happen to be the standard for most prehospital agencies, and hospital systems.  They say and we do.  So what are we going to be doing now?

This year should not be bringing about any mega changes.  The direction has stayed the same for the most part.

Where do the updates come from?

ILCOR - The International Liaison Committee on Resuscitation
Process for Evidence Evaluation

The publication of the 2010 International Consensus on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) Science with Treatment Recommendations (CoSTR) will represent the scientific consensus of experts from a variety of countries, cultures and disciplines. Internationally recognized experts were brought together by the International Liaison Committee on Resuscitation (ILCOR) to evaluate and form an expert consensus on all peer reviewed scientific studies related to CPR.

To achieve this goals, ILCOR is conducting systematic reviews and updates of scientific evidence supporting resuscitation treatment recommendations. More than 500 resuscitation scientific topics will undergo evidence-based review. This process represents the most comprehensive, systematic review of the resuscitation literature to date.

The worksheets posted at this site represent the first step of an international consensus evidence evaluation process that will culminate in the publication of the 2010 International Consensus on CPR and ECC Science with Treatment Recommendations. In addition, resuscitation council-specific guidelines will also be published based on this international science consensus. Worksheet authors and expert reviewers worked very hard to present the information objectively.

The information contained in these worksheets will be presented and discussed between now and early 2010. In early 2010, the International CPR Consensus Conference will convene to allow final presentation and discussion of these worksheets, leading to evaluation and consensus by respective ILCOR Task Forces.
Readers are cautioned that these worksheets are a preliminary review and do not represent any ILCOR Task Force or Resuscitation Council recommendations.

ILCOR recognizes that the integrity of the evidence evaluation process depends on successfully managing real and perceived conflict of interest. ILCOR has policies in place to manage conflict of interest.
The 2010 evidence evaluation and science review process will culminate with the International CoSTR Conference in early 2010, in Dallas, Texas.

A separate publication covering guideline recommendations will be published by each resuscitation council.

So what does this all mean?

The AHA is part of an international committee that uses a systematic review system to scan through all the most valuable research available.  The research is graded by how useful an unbiased it is, and then recommendations are made based upon a compilation of the results.  The package all of this up in a nice-looking book, packed with a bunch of fancy flow charts, tables, and algorithms, and we buy it.

Link to the questions asked for 2010

Time of old

Amiodarone - Back in 2000 Amiodarone was given a class IIb recommendation from AHA.  This was a push from, who else, the manufacturers of Amio.  This happened synchronously with the changing of Lidocaine from a class IIb to an indeterminate rating.  This occurred after a study showed that Amiodarone improved the number of cardiac arrest that regained pulses.  This was accepted by many, and all the better, Amio works in atrial and ventricular arrhythmias--yippee.

The facts:

  • Amiodarone improved the amount of people that regained pulses, but not the amount of cardiac arrests that survived to discharge.  No more people are surviving on Amio compared to Lidocaine.   AHA knows this now, and has known this for a while.  
  • AHA says that an "indeterminate" rating is no different from class IIb.  So why the change?  Because class IIb sounds a whole lot better when your selling a new drug.

So does this mean we are going back to lidocaine?  Not sure, because there isn't any evidence that lidocaine is any better either--should we confuse everyone more?  In fact, there is no evidence that any dysrhythmic does anything beneficial in cardiac arrest.  That's right, no quality evidence supporting beneficial effects of dysrhythmics.  Want some more?  NO DRUGS administered in cardiac arrest have any supporting evidence!

Olasveengen TM, Sunde K, Brunborg C, et al. Intravenous drug administration
during out-of-hospital cardiac arrest. JAMA 2009;302:2222-2229.
Despite the traditional use of intravenous medications such as vasopressors and antiarrhythmics for victims of cardiac arrest, there is actually very little evidence to support these therapies. On the contrary, a recent multicenter center study demonstrated that the use of intravenous medications that are advocated in standard advanced cardiac life support (ACLS) guidelines was ineffective at improving survival of patients with out- of-hospital cardiac arrest (1). Olasveengen and colleagues now add further support to the contention that the use of intravenous medications in victims of non-traumatic cardiac arrest is not associated with improvements in meaningful outcomes. The authors performed a prospective randomized trial of consecutive adults with non-traumatic cardiac arrest that were treated within their emergency medical services (EMS) system in Oslo between 2003 2008. Patients were randomized to either receive standard ACLS therapies with intravenous drug administration (IV group) or ACLS therapies without any intravenous drugs (no IV group). A total of 851 patients were included in the study, 418 patients in the IV group and 433 in the no IV group. The researchers found there was an increase in survival to hospital admission with return of spontaneous circulation in the IV group vs. the no IV group (32% vs. 21%, P < 0.001). However, there was no difference between the IV group vs. the no IV group in terms of survival to hospital discharge (10.5% vs. 9.2%, P = 0.61), survival with favorable neurological outcome (9.8% vs. 8.1%, P = 0.45), or survival at 1 year (10%  vs. 8%, P = 0.53). The results demonstrate that with the use of IV ACLS medications, patients simply die in the hospital rather than in the ED. Practically speaking, this amounts to increased intensive care unit bed utilization, hospital resource utilization, and expenses; but without any increase in meaningful survival. In this era of ED and hospital overcrowding and the increasing demand for cost-effectiveness in medical therapies, Stiell’s and Olasveengen’s studies should force us to consider that the use of IV medications for patients in cardiac arrest should be the exception rather than the rule…or guideline. 
1. Stiell IG, Wells GA, Field B, et al. Ontario Prehospital Advanced Life Support Study Group. Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med 2004;351:647-656.
Back to Amiodarone 2010:
Evidence from 1 RCT demonstrates the benefit of amiodarone over placebo for shock refractory or recurrent VT/VF for the endpoint of survival to hospital admission, but not to survival to hospital discharge. Retrospective trials show that lidocaine may be more beneficial than placebo, but selection bias mars these trials. In trials that directly compare amiodarone to lidocaine, patients administered amiodarone generally do better in short term results (ie survival to hospital admission), but no trial has shown an improvement in overall survival (Dorian P 2002 p884, Somberg J 2002 p853). 
These trials were performed before the benefits of hypothermia was known, thus they did not incorporate this now proven therapy which improves survival after ROSC. Whether survival to hospital discharge and neurologic survival could be improved with amiodarone and subsequent hypothermia is not known. If that is the case then a stronger argument for amiodarone could be made; if that is not the case then an argument could be made to not give an AAD at all.

CPR Before Defibrillation

It was taught, back in 2005 by AHA, that we need to prime the pump.  It was theorized that performing early defibrillation has no benefit because the heart was not being adequately perfused.  This lead to a 2 minutes of CPR prior to shocking in an unwitnessed arrest rule.  This is what we, who are AHA compliant, are doing.

Two randomized controlled trials (LOE I) (Baker 2008 p424; Jacobs 2005 p39) demonstrated no improvement in ROSC or survival to hospital discharge in patients suffering out-of-hospital VF or pulseless VT who received CPR by EMS personnel for a period of 1.5 to 3 minutes before defibrillation, regardless of EMS response interval being greater or less than 5 minutes. One case series study (LOE IV) (Campbell 2007 p229) also failed to demonstrate improvements in ROSC or survival to hospital discharge with bystander versus no bystander CPR before defibrillation.
One randomized controlled trial (LOE I) (Wik 2003 p1389) and clinical trial (LOE III) (Cobb 1999 p1182) identified overall similar findings however improvements in ROSC, survival to hospital discharge and neurological outcome were observed in patients where the EMS response interval was greater than 4 to 5 minutes.

Evidence from one LOE 1 study (Wik 2003, 1389), one LOE 3 study (Cobb 1999, 1182) and five LOE 5 studies (Berg 2004, 1352; Kolarova 2003, 2022; Menegazzi 1993, 235; Menegazzi 2004, 926; Niemann 1992, 281) support the strategy to delay defibrillation to give BLS first for 1,5 to 8 minutes, in particular when the delay to ambulance arrival exceeds 5 minutes and no BLS is given before ambulance arrival. Evidence from two LOE 1 studies (Baker 2008, 424; Jacobs 2005, 39), one LOE 3 study (Campbell 2007, 229) and nine LOE 5 studies (Berg 2004, 1352; Yakaitis 1980, 157; Menegazzi 2003, 261; Menegazzi 2000, 31; Seaberg 2001, 301; Kolarova 2003, 2022; Niemann 2000, 543; Menegazzi 1993, 235; Rittenberger 2008, 155) do not support this strategy and are neutral. One LOE 5 study (Indik 2009, 179) gave direct evidence for the opposite strategy

Level of evidence - all that LOE stuff you see above is a reference to the grade the mentioned study received by the reviewer.
Randomised Controlled Trials:
These studies prospectively collect data, and randomly allocate the patients to intervention or control groups. 
Studies using concurrent controls without true randomisation:
These studies can be:
· experimental - having patients that are allocated to intervention or control groups concurrently, but in a non-random fashion (including pseudo-randomisation: eg. alternate days, day of week etc), or
· observational – including cohort and case control studies
A meta-analysis of these types of studies is also allocated a LOE = 2. 
Studies using retrospective controls:
These studies use control patients that have been selected from a previous period in time to the intervention group. 
Case series: A single group of people exposed to the intervention (factor under study), but without a control group. 
As with other categories of Levels of Evidence, we have used LOE 5 to refer to studies that are not directly related to the specific patient/population. These could be different patients/population, or animal models, and could include high quality studies (including RCTs).
So according to the evidence, we may need more evidence.  However, there isn't much support to the current guidelines.  Once again, do we change this back and confuse more people when we are uncertain if outcomes will improve?

Cardiocerberal Resuscitation or Cardiopulmonary Resuscitation?

Should EMS be doing chest compression only CPR?  This is a good question when considering primary cardiac arrest.  We know that primary respiratory arrest should involve aggressive airway management.
Six fair to good LOE 5 animal studies (Berg 1993, 1907; Berg 1997, 1635; Berg 2001, 2464; Ewy 2007, 2525; Kern 1998, 179; Kern 2002, 645) have shown comparable or better outcomes with continuous chest compression CPR as compared with interrupted compressions for ventilation in nonasphyxial cardiac arrest and in concept support such a change in resuscitation strategy. However animal models do not necessarily mimic the anatomical or arrest features of humans, and for these reasons arguably may be less applicable to human resuscitation. Clinical evidence from three retrospective cohort LOE 3 studies in adults suffering from cardiac arrest (Bobrow 2007, 1158; Kellum 2006, 335; Kellum 2008, 244) showed that provision of chest compressions in the absence of rescue breathing by trained professional (EMS) providers led to an improvement in survival to hospital discharge compared to provision of chest compressions with rescue breathing. However, these studies had methodological shortcomings that limit the ability to determine whether the improvements in survival were attributable to the provision of chest compression-only CPR in the absence of rescue breathing, including the lack of randomization, the implementation of other resuscitation protocol changes that may have affected outcomes, or simply a stronger clinical emphasis on the provision of good CPR. The remainder of clinical studies addressing this issue evaluated the outcome from continuous chest compression versus interposed ventilation CPR by untrained laypersons (bystander CPR),and did not directly address provision of care by trained professionals.
So there are studies out there, just maybe not enough--once again.  There is also research on different compression:ventilation ratios showing promising data.  Guess we will find out what really happens in October.

More of the same

There is a lot more evidence out there advocating chest compressions.  No pulse checks, just compressions.  More and more compressions.  Push hard and push fast.  Good chest compressions.  Are you getting all of this?

Therapeutic hypothermia is gaining more popularity.  The evidence is outstanding.
Who to cool?
Evidence from one good randomized trial (LOE 1) (HACA, 2002, 549) and a pseudo-randomised trial (LOE 2) (Bernard, 2002,557) demonstrate improvement in neurological outcome after discharge from hospital in patients who had an out-of-hospital VF cardiac arrest, who were still comatose, and who were cooled within minutes to hours after return of spontaneous circulation to 32-34ºC for 12-24 hours. Two studies with historical control groups (LOE 3) showed improvement in neurological outcome after therapeutic hypothermia for comatose survivors of VF cardiac arrest (Belliard, 2007, 252; Castrejon, 2009, 733) One small (n = 30) randomized trial (LOE 1) showed reduced plasma lactate values and oxygen extraction ratios in a group (n =16) of comatose survivors after cardiac arrest with asystole or PEA who were cooled with a cooling cap (Hachimi-Idrissi, 2001, 275). Six studies with historical control groups (LOE 3) showed benefit after therapeutic hypothermia in comatose survivors of OHCA after all rhythm arrests (Bernard, 2007, 146; Oddo, 2006, 1865; Busch, 2006, 1277; Sunde, 2007, 29; Storm, 2008, R78; Don, 2009 3062). One studies with historical controls showed better neurological outcome after VF cardiac arrest but no difference after cardiac arrest from other rhythms (Bro-Jeppesen, 2009, 171). Two non-randomised studies with concurrent controls (Arrich, 2007, 1041; Holzer, 2006, 1792) indicate possible benefit of hypothermia following cardiac arrest from other initial rhythms in- and outof-hospital.

How to cool?
Nine case series (LOE 4) indicate that cooling can be initiated safely with intravenous ice-cold fluids (30 ml/kg of saline 0.9% or Ringer’s lactate) (Kliegel, 2005, 347; Kliegel 2007, 56; Bernard, 2003, 9; Virkkunen, 2004, 299; Kim, 2005, 715 ; Jacobshagen, 2009; Kilgannon, 2008; Spiel, 2009; Larsson, 2010;). Two randomised controlled trials (Kim, 2007, 3064; Kamarainen, 2009, 900), one study with concurrent controls (LOE 2: Hammer, 2009, 570) and three cases series (LOE 3) (Kamarainen,2008, 360;Kamarainen, 2008, 205) indicate that cooling with IV cold saline can be initiated in the pre-hospital phase.

More For Post-Arrest 

There is evidence that patients who are resuscitated from primary cardiac arrest should be immediately cathed.
The significance of this new literature cannot be overstated. If further studies confirm these findings, it would strongly argue for enormous changes in prehospital systems of care to recommend that all survivors of primary cardiac arrest should be immediately transported to hospitals that have the capability of performing urgent PCI in conjunction with therapeutic hypothermia. Based on the current literature, it certainly seems advisable that emergency health care practitioners that care for resuscitated victims of primary cardiac arrest should engage in conversations with cardiology consultants and urge them to take an aggressive approach to PCI in these patients.
What does this mean for us?  Post-arrest 12-lead ECGs for now.  In the future, this may mean that we bypass non-PCI facilities with our post-arrest patients.  If you think this will last long, you are wrong.  Post-arrest patients are high dollar patients.  Just think about all of the work-ups done on these patients.  Don't think that the non-PCI hospitals won't be rushing to find a way around this.  Will this mean more PCI centers?  Probably not, because all of the other cardio-intervention seeking patients end up with big medical bills too--but who knows.

Shocking Stuff

So even though AHA came out and said that their initial recommendation for biphasic defibrillators is not backed by any evidence, there may be an actual benefit to having them.  There is evidence supporting what I am about to tell you, but it may not make it into the 2010 update.  I think it will though.  It goes against what we have all learned.  Remember "I'm clear, you're clear, we're all clear!"

There is no harm to a rescuer performing chest compressions, when defibrillation is performed using a biphasic monitor.

That's right.  It has been said that more electricity passes through your body on one of those scales that checks your BMI than touching a patient when they are getting shocked.  It has to be a biphasic defibrillator though.

So that's all so far.  Go scan through the worksheets if you'd like.  There is a ton of good research available.  We can only assume, as of yet, what the final recommendations will be.  

At the Florida Emergency Physicians' second annual symposium on critical care in the emergency department, Dr. Amal Mattu (yes, I am mentioning him once again) presented most of these updates.  This motivated me to research and share them with you.    


Firefighter/Paramedic said...

Great post. Can't wait to see what they've changed this time!

Adam Thompson, EMT-P said...

Thanks, I think they are headed in the right direction. There seems to be a lot of good evidence being reviewed. I never read through the actual worksheets in the past, so I am not quite sure how to compare the quality of these updates to the past. In 2015 though, I will have a much better understanding of the process and validity of the reviews.