Chronicles of EMS, A Seat at the Table takes on CPR effectiveness.  The Las Vegas video that they mention can be found below as well.  Keep up the good work Justin and Mark!

Side note - ILCOR, The International Liaison Committee On Resuscitation has not found any supporting evidence for the Autopulse.  They are the ones whom do the research for AHA.  Also, transporting patients without a pulse should be re-looked at by any agency performing this practice.  The initial treatment at the ER will not differ from the treatment we provide at the scene per ACLS guidelines.  Why not give the patient the best chance possible.  If they don't get a pulse back on scene, it is probably never going to come back--that's just the facts.

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:

CONSENSUS ON SCIENCE:
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.

CONSENSUS ON SCIENCE:
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.

LOE 1
Randomised Controlled Trials:
These studies prospectively collect data, and randomly allocate the patients to intervention or control groups. 

LOE 2
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. 

LOE 3
Studies using retrospective controls:
These studies use control patients that have been selected from a previous period in time to the intervention group. 

LOE 4
Case series: A single group of people exposed to the intervention (factor under study), but without a control group. 

LOE 5
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.

CONSENSUS ON SCIENCE
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.

CONSENSUS ON SCIENCE: 

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.  

Allow me to introduce myself. My name is Chris Kaiser, or Ckemtp, and I write the EMS blog http://www.lifeunderthelights.com/ - I am a Nationally Registered Paramedic holding licensure in Illinois, Iowa, and also in Wisconsin. A few months ago I was asked to become a contributor to write for this blog and I jumped at the chance to intermingle my stuff with the venerable names here. Unfortunately, it has taken me a while to get something up here with the work needed to move from my old site to the new site. Today I'm fixing that and I would like to repost this article here with a few updates. I hope you find it educational.

Visitors to my blog probably know that at my ambulance service we tend to bring back a lot of codes. I talk about it a lot. Back in 2004 our medical director, Dr. Michael Kellum, got us involved in a “Demonstration Project” to bring Continuous Compression CPR or Cardiocerebral resuscitation to a rural area. Since that time, the results have been more than dramatic. Depending on what statistics you look at, we may be “Saving” almost 50% of witnessed arrests found to be in ventricular fibrillation.

It’s all explained at http://www.callandpump.org/, but if you want to go right to the whitepaper that explains what we do, why we do it, and how it’s done then you want to go here: http://callandpump.org/assets/Proposal_Current.pdf – This link is explains the demonstration project initiated by Dr. Kellum et al. in the two county area that I work in. This paper was published in 2004 at the beginning of the project.

This is a link to the results published in the Annals of Emergenc Medicine in 2008 – http://www.ncbi.nlm.nih.gov/pubmed/18374452?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

You may be interested in this part:

“RESULTS: In the 3 years preceding the change in protocol, there were 92 witnessed arrests with an initially shockable rhythm. Eighteen patients survived (20%) and 14 (15%) were neurologically intact. During the 3 years after implementation of the new protocol, there were 89 such patients. Forty-two (47%) survived and 35 (39%) were neurologically intact. CONCLUSION: In adult patients with a witnessed cardiac arrest and an initially shockable rhythm, implementation of an out-of-hospital treatment protocol based on the principles of cardiocerebral resuscitation was associated with a dramatic improvement in neurologically intact survival.”

This is good stuff. Remember, the above is only reflective of those included in the study, who are “Witnessed arrest(s) with an initially shockable rhythm”. Anecdotally, I’ve personally attended those that were not in a shockable rhythm and witnessed greater effectiveness as well.

Here’s the short version of our protocols for Witnessed V-Fib Arrest: (and for those of you who want more, email me at: proems1@yahoo.com and I will be happy to send you a copy of the protocols)

We follow an acronym called MCMAID in our resuscitation protocols, it stands for:

Metronome – We carry a metronome in our monitor/defibrillator bags that clicks out at 100 beats per minute. We are to compress at 100bpm. No more, no less. This metronome keeps us on rhythm and reminds us to be on the chest.

Compressions – 100 compressions per minute. Do not stop. Initially, we are to administer 200 compressions (2 minutes) before our first shock. We are to limit any interruptions in compressions absolutely as much as possible, charging our defibrillators while compressions are ongoing and recognizing V-fib through the compressions if possible. Compress hard and deep, completely releasing tension on the chest upon recoil to maximize the compression and decompression of the chest.

Monitor – Place the monitor on the patient using fast patches. Do not stop the 200 compression cycles to determine the rhythm. Shock at max joules biphasic. If you can anticipate V-Fib, charge the defib during the compressions and only stop long enough to clear for the shock. Don’t check the pulse, get right back to compressions.

Airway – Initially, a BLS airway will be placed in the patient and a non-rebreather oxygen mask will be placed on the patient. If the airway must be controlled by more advanced means to protect and ensure a patent airway, now is the time to do so.

Intravenous Access – Most of the time, this is accomplished through the means of the Ez-IO drill that we carry and love. (See: Alternative Circulatory Access Strategies – Hi Ho IO) This can also be obtained through peripheral or EJ IV access.

Drugs – Epinephrine 1:10,000 1mg IVasopression 40 IU, Amiodarone 300mg, then Epinephrine 1:10,000 1mg q 3-5min. If refractory, we may give an additional 150mg Amiodarone IV.

To see the full MCMAID CCR protocol (I put it up in a post) you can see it by clicking here.

Dr. Kellum came down again for our monthly training recently and let us know the latest breakthroughs and orders in the project. He is stressing the importance of End-Tidal CO2 (ETCO2) monitoring and states that no pulse check is necessary without a spontaneous increase in ETCO2. He expects every intubated (or combitubed) patient to have ETCO2 monitoring in place.

He also expects that we will monitor ETCO2 readings as a way to prove effectiveness of compressions. Rescuers who cannot get ETCO2 readings consistent with other personnel when providing compressions shouldn’t be doing compressions.

Rescuers should switch off compressions EVERY ONE MINUTE whenever possible. This is providing some fantastic results in preliminary trials.

He also stated that the effectiveness of the CCR protocols are showing a marked increase in refractory V-fib. He hinted that the protocols might soon show a need for thrombolytic use in treatment of refractory V-Fib.

Stay tuned folks, I am happy as heck to be included in this. I will bring updates, with permission, as many times as I get them. You can find more information on this on http://www.lifeunderthelights.com/. It's truly exciting stuff.

Mild therapeutic hypothermia (32 degrees C-34 degrees C) is the only therapy that improved neurological outcome after cardiac arrest in a randomized, controlled trial. Induced hypothermia after successful resuscitation leads to one additional patient with intact neurological outcome for every 6 patients treated. It protects the brain after ischemia by reduction of brain metabolism, attenuation of reactive oxygen species formation, inhibition of excitatory amino acid release, attenuation of the immune response during reperfusion, and inhibition of apoptosis. Potential side effects such as infections have to be kept in mind and treated accordingly. Mild hypothermia is a safe and effective therapy after cardiac arrest, even in hemodynamically compromised patients and in patients undergoing percutaneous coronary intervention. Its use is recommended by the American Heart Association and the International Liaison Committee on Resuscitation for unconscious adult patients with spontaneous circulation after out-of-hospital ventricular fibrillation cardiac arrest. Further research is needed to maximize its potential benefits.

BACKGROUND: Local hypothermia induced by intravascular infusion of cold saline solution effectively reduces brain damage in stroke. We further determined the optimal temperature of local hypothermia in our study. METHODS: Seventy-eight adult male Sprague Dawley rats (260 - 300 g) were randomly divided into 3 groups: group A, ischemia/reperfusion without cold saline infusion (n = 26) (control group); group B, infusion with 20 degrees C saline before reperfusion (n = 26); group C: infusion with 10 degrees C saline before reperfusion (n = 26). In each group, we chose 15 rats for monitoring physical indexes and the temperature of the brain (cortex and striatum) and body (anus), measurement of brain infarction volume, assessment of neurological deficits and the survival rate of reperfusion at 48 hours. Another 8 rats from each group was chosen for examining brain edema, another 3 from each group for histological observation by electron microscopy (EM) and light microscopy (LM) at 48 hours after reperfusion. RESULTS: There was no significant difference among the 3 groups for physical indexes during the examination (F((2, 45)) = 0.577, P = 0.568; F((2, 45)) = 0.42, P = 0.78 for blood pressure and blood gas analysis, respectively). The brain temperature was significantly reduced in the group C compared to the other groups (F((2, 45)) = 37.074, P = 0.000; F((2, 45)) = 32.983, P = 0.000, for cortex and striatum temperature respectively), while the difference in rectal temperature between group A and B or C after reperfusion was not significant (F((2, 45)) = 0.17115, P = 0.637). And the brain infarct volume was significantly reduced in group C (from 40% +/- 10% in group A, 26% +/- 8% in group B, to 12% +/- 6% in group C, F((2, 45)) = 43.465, P = 0.000) with the neurological deficits improving in group C (chi(2) = 27.626, P = 0.000). The survival rate at 48 hours after 10 degrees C and 20 degrees C saline reperfusion was increased by 132.5% and 150%, respectively, as compared to the control group (chi(2) = 10.489, P = 0.005). The extent of the brain edema showed no significant difference (F((2, 21)) = 0.547, P = 0.587) after cold saline infusion compared to the control group. No obvious vascular injury was found by electron or light microscopy in either infusion group. CONCLUSIONS: Regional hypothermia with 10 degrees C cold saline infusion can significantly decrease the infarction volume, improve the neurological deficits, and 10 degrees C seems to be the optimal temperature in inducing a cerebral protection effect during stroke. This procedure could be adopted as a further treatment for acute stroke patients.

[Pubmed 4]

Hypothermia is considered nature's "gold standard" for neuroprotection, and its efficacy for improving outcome in patients with hypoxic-ischemic brain injury as a result of cardiac arrest is well-established. Hypothermia reduces brain edema and intracranial pressure in patients with traumatic brain injury. By contrast, only a few small pilot studies have evaluated hypothermia as a treatment for acute ischemic stroke, and no controlled trials of hypothermia for hemorrhagic stroke have been performed. Logistic challenges present an important barrier to the widespread application of hypothermia for stroke, most importantly the need for high-quality critical care to start immediately in the emergency department. Rapid induction of hypothermia within 3 to 6 hrs of onset has been hampered by slow cooling rates, but is feasible. Delayed cooling for the treatment of cytotoxic brain edema does not provide definitive or lasting treatment for intracranial mass effect, and should not be used as an alternative to hemicraniectomy. Sustained fever control is feasible in patients with intracerebral and subarachnoid hemorrhage, but has yet to be tested in a phase III study. Important observations from studies investigating the use of hypothermia for stroke to date include the necessity for proactive antishivering therapy for successful cooling, the importance of slow controlled rewarming to avoid rebound brain edema, and the high risk for infectious and cardiovascular complications in this patient population. More research is clearly needed to bring us closer to the successful application of hypothermia in the treatment for stroke.

[Pubmed 5]

OBJECTIVE: Hypothermia has long been known to be a potent neuroprotectant. In this mini-review, we highlighted clinical experience that hypothermia protects the brain from cerebral injury. We discussed the clinical practice of hypothermia in ischemic stroke. RESULTS: Multiple factors play a significant role in the mechanisms. Clinical application drew first from two clinical trials with comatose patients after cardiac arrest is attractive. The Australian and European study have led to renewed interest in these patients. More and more evidences bring the insight into its effects on cerebral ischemia. The type of cooling technique to be used, the duration of cooling and speed of rewarming appear to be key factors in determining whether hypothermia is effective in preventing or mitigating neurological injury. Although until now, there are no clear therapeutic standards of the parameters in therapeutic hypothermia, it is well accepted that cooling should be initiated as soon as possible. By combining hypothermia with other neuroprotectants, it may be possible to enhance protective effects, reduce side effects and lengthen the maximum time. CONCLUSION: In addition to its neuroprotective properties, hypothermia may extend the therapeutic window for other neuroprotective treatment. Thus, combination therapies with neuroprotective, anti-inflammatory and thrombolytic agents are likely to be investigated in the clinical setting in the future.

Pubmed

PURPOSE OF REVIEW: To discuss recent findings surrounding the role of ventilation during cardiopulmonary resuscitation for individuals with out-of-hospital primary cardiac arrest. RECENT FINDINGS: Active assisted ventilation during primary cardiac arrest may not always be beneficial and, in some circumstances, may lead to worse outcomes. By interrupting chest compressions and thereby decreasing vital organ perfusion, rescue breathing may be deleterious. In addition to the time required to administer breaths, the delay due to the insertion of advanced airways, even by well trained individuals, is often extensive. Furthermore, once intubation is completed, excessive hyperventilation occurs frequently, even by recently trained medical providers. Although most experts agree that excessive ventilation is harmful during out-of-hospital cardiac resuscitation, the optimal rate, tidal volume, timing, and technique of ventilation is still unknown. There is increasing evidence that, in patients with witnessed arrests and a shockable rhythm, the optimal form of ventilation is passive oxygen insufflation. SUMMARY: Assisted ventilation during the initial provision of cardiopulmonary resuscitation is less important than previously believed. It is hypothesized that, by training prehospital medical providers to utilize passive oxygen insufflation for individuals with primary cardiac arrest, critical organ perfusion will increase and, therefore, survival after out-of-hospital cardiac arrest will improve.

Background: Several investigators have emphasized the positive effect of hypothermia therapy on patients who have suffered from cardiac arrest. Salvaging patients from circulatory collapse is a pivotal task, but it is unclear whether additional hypothermia can practically contribute to an improvement in the neurological outcome. Methods and Results: Since December 2005, our hospital has been using hypothermia therapy. Forty-six comatose patients after recovery of spontaneous circulation were consecutively enrolled in the present study. Twenty-five of the enrolled patients received hypothermia therapy and 21 did not because they were treated prior to 2005. The time from collapse to spontaneous circulation (P=0.09), the rates of performance of bystander CPR (P=0.370) and presence of a witnessed collapse (P=0.067) were not significantly different between the recovery group (n=28) and the non-recovery group (n=18). The additional hypothermia therapy was an independent predictor of neurological recovery (P=0.005, OR 6.5, 95%CI 1.74-24.27). The recovery rate was significantly higher in patients who received hypothermia therapy (80%) compared to those who did not (38%). Conclusions: Hypothermia therapy is very useful for treating patients who have had an out-of-hospital cardiac arrest; it should be induced rapidly and smoothly.

An interesting story about a different in hospital cooling method:JEMS Webcast - Brent Myers, the medical director for Wake EMS, delivers an excellent presentation.

Most recent studies from Pubmed:

[3]Mild resuscitative hypothermia has been shown to improve neurological outcome after cardiac arrest presenting with ventricular fibrillation (VF) due to cardiac causes. We describe the experience of inducing mild hypothermia in three patients with non-cardiac causes of arrest and long delays before a return of spontaneous circulation (ROSC). In one patient, extreme metabolic acidosis due to inadvertent oesophageal intubation complicated therapy, and the role of point-of-care diagnostics in the prehospital setting is briefly discussed. All patients survived to discharge from hospital, and neuropsychological examinations revealed good recovery. It is concluded that mild resuscitative hypothermia may be beneficial also in patients with obvious non-coronary causes for cardiac arrest.

While there is limited research on the topic of induced hypothermia, the research available is heavily in favor of the procedure. When I hear physicians criticize the immaturity of this therapy, I laugh thinking about epinephrine. As RM's last few posts have implied, Epi has been around for quite a while and there is no evidence in support of its use in cardiac arrest protocols. Would those physicians be so critical of Epi?

Here are two protocols for induced hypothermia following return of spontaneous circulation (ROSC).