I have put together a capnography tutorial for your education and enjoyment. The videos below are the capnography tutorial. There are 7 lessons, consisting of relatively short videos.
Adam Thompson, EMT-P
I have put together a capnography tutorial for your education and enjoyment. The videos below are the capnography tutorial. There are 7 lessons, consisting of relatively short videos.
Adam Thompson, EMT-P
This is an interesting study for several reasons. One is the ability of the authors to act out parts of Through the Looking-Glass. VF and VT are Ventricular Tachycardia and Ventricular Fibrillation.
If life-threatening VF or VT persists despite repeated deﬁbrillation shocks, an additional antiarrhythmic drug is required.
The next paragraph points out that there is no requirement according to ACLS.
The American Heart Association guideline for advanced cardiac life support (ACLS) states that when VF/pulseless VT persists after two to three shocks plus CPR and administration of a vasopressor, the physician should consider administering an anti-arrhythmic such as amiodarone, and lidocaine may be considered if amiodarone is unavailable.1 
Believing that should consider administering is the same as an additional antiarrhythmic drug is required requires the same lack of illogic as used by the Queen, when instructing Alice to practice believing impossible things.
Then there are the obvious questions. Why compare nikefelant with lidocaine? Why not compare nikefelant with amiodarone? Why not compare nikefelant with an antiarrhythmic that is more effective than amiodarone – procainamide, sotalol, or ajmaline?
Lidocaine is probably used because the IRB (Institutional Review Board) would consider it unethical to have a placebo group. Lidocaine is the placebo, but with less safety than the placebo.
It was by comparing amiodarone with lidocaine that ACLS ended up including amiodarone for VT/VF cardiac arrests. That was a huge boon for Wyeth. We were told that the improved survival to admission was important. We were told that survival studies – the only studies that matter in resuscitation – were being done. We have had only silence since then.
We should conclude that amiodarone does not improve survival.
No. That is not the right conclusion. If amiodarone produced survival as good as placebo, then that study would have been published and used to justify giving amiodarone. At least we are doing something! That is what people want to believe in.
The only reasonable conclusion is that Wyeth did not publish the results because the survival in the amiodarone group was significantly worse than in the placebo group, or Wyeth stopped the study early, because it was trending toward statistically significant harm from amiodarone.
If the study never reaches statistical significance, they can always rely on there being no proof of harm. That is what we have now and there are plenty of people claiming that no proof of harm means obvious benefit.
We have a lot of ignorant/willfully ignorant people encouraging us to just give drugs because we cannot prove that these drugs are harmful. We cannot provide evidence that the drugs are harmful, because it is almost impossible to approve a placebo-controlled study to find out. The IRBs claim that it would be unethical to deprive patients of the Standard Of Care, no matter how harmful that Standard Of Care may be. If the IRBs approve a study, the politicians oppose the study.
There were some interesting differences between the lidocaine and nukefalant groups.
The number of shocks before study-drug administration did not differ between the two arms, although epinephrine use before study-drug administration was signiﬁcantly higher in the lidocaine arm (Table 2).
Nikefalant 6/27 – 22.2%
Lidocaine 20/28 – 71.4%
With a p value of <0.001
According to ACLS, an antiarrhythmic should not be considered until after a pressor is considered.
Patients with nifekalant were more likely to have ROSC compared with patients with lidocaine (Table 3). However, there was no difference in 1-month survival or survival to hospital discharge between the nifekalant arm and the lidocaine arm.
The overall outcome, such as survival rate, of patients with shock-resistant VF or VT is poor regardless of the pharmacological intervention. Nevertheless, termination of VF or VT and recovery of ROSC by nifekalant is important in the initial stage of resuscitation, because we cannot rescue the patients unless VF or VT is converted.
They assume that the VF/VT will not be converted without a drug.
They assume that converting more VF/VT will lead to more survival even though there continues to be absolutely no evidence to support this hope.
It is reasonable to assume that the short-term thrill of conversion of VF/VT to a better rhythm comes at the expense of long-term harm to the patient.
We need to stop falling for feel good endpoints that encourage us to harm our patients.
If others are NOT helping their patients with these drugs, we want to be NOT helping our patients, too!
‘I can’t believe THAT!’ said Alice.
‘Can’t you?’ the Queen said in a pitying tone. ‘Try again: draw a long breath, and shut your eyes.’
Alice laughed. ‘There’s no use trying,’ she said: ‘one CAN’T believe impossible things.’
‘I daresay you haven’t had much practice,’ said the Queen. ‘When I was your age, I always did it for half-an-hour a day. Why, sometimes I’ve believed as many as six impossible things before breakfast.
 Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia.
Shiga T, Tanaka K, Kato R, Amino M, Matsudo Y, Honda T, Sagara K, Takahashi A, Katoh T, Urashima M, Ogawa S, Takano T, Kasanuki H; Refractory VT/VF, Prospective Evaluation to Differentiate Lidocaine Efficacy from Nifekalant (RELIEF) Study Investigators.
Resuscitation. 2010 Jan;81(1):47-52. Epub 2009 Nov 13.
PMID: 19913983 [PubMed - indexed for MEDLINE]
 Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
PMID: 21745533 [PubMed - in process]
This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.
In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.
Continuing, after a 6 month delay, a discussion of an EMS 12 Lead article from Part I. ACLS (Advanced Cardiac Life Support) recommends charging the defibrillator during compressions. This is no less of a recommendation than giving epinephrine. How many people ignore ACLS guidelines for compressions during charging, but claim that it is evil to disobey anything ACLS recommends on epinephrine, amiodarone, or ventilations?
Analyses of VF waveform characteristics predictive of shock success have documented that the shorter the time interval between the last chest compression and shock delivery, the more likely the shock will be successful.141 A reduction of even a few seconds in the interval from pausing compressions to shock delivery can increase the probability of shock success.142 
Extra pauses in compressions add to the time without compressions.
If the medic/nurse/doctor using a manual defibrillator recognizes a shockable rhythm, why not provide compressions while charging the defibrillator?
Some people will say that this is dangerous.
But if someone accidentally delivers a shock during compressions, people will be killed!
In a systematic review, Hoke et al. summarized 29 reports of accidental deﬁbrillator discharges, of which only 15 occurred during resuscitation attempts.21 Symptoms included tingling sensations, discomfort, and minor burns, but no long term effects or major consequences were reported.
Where are the dead bodies we hear so much about?
Where are the medics/nurses/doctors needing to be defibrillated back to life?
There was only one incident where a shock was delivered while a rescuer was actively performing chest compressions. However, the compression transcript continued without any visible change to CPR administration, suggesting that the rescuer was unaffected by the event. Review of clinical records and audio transcripts revealed no evidence of inadvertent shocks to rescuers. In addition, there was no signiﬁcant difference in the incidence of inappropriate shocks to patients associated with charging during compressions (20.0% vs 20.1%; p = 0.97). 
In this study, there was one case of a shock being delivered during compressions, but nobody seems to have been affected by this shock.
What happened to the automatic death that ACLS instructors spend so much time describing?
Where is the evidence?
In the current study, charging during compressions decreased median pre-shock pause by over 10 s, which previous studies suggest could have a dramatic effect on clinical outcomes. We previously reported an almost two-fold increase in the chances of successful deﬁbrillation for every 5 s reduction in the pre-shock pause.9 Similarly, Eftestøl et al. found that a 10 s hands-off period prior to deﬁbrillation would roughly halve the probability of obtaining ROSC.6 
The risk to rescuers appears to be minimal, but the possible benefit to patients may be dramatic.
The difference in time without compressions is significant.
Interestingly, we found that the most efﬁcient technique with regard to minimizing pauses was not the AHA recommended method of pausing to analyze, resuming CPR to charge, and then pausing again to deﬁbrillate. Rather, charging at the end of every 2 min CPR cycle in anticipation of a shockable rhythm and then pausing only once, brieﬂy, to both analyze and either shock or disarm was associated with signiﬁcantly shorter total pause duration in the 30 s preceding deﬁbrillation. 
If we see asystole, we do not deliver a shock. We cancel the shock.
If we see PEA (Pulseless Electrical Activity, such as sinus rhythm, sinus tachycardia, sinus bradycardia, or any other non-shockable rhythm), we do not deliver a shock. We cancel the shock.
Cancelling the shock is not going to be the same for each defibrillator, but we do need to know how to cancel the shock for each machine we use. We can read the instructions.
We can turn on the monitor, charge it up to the setting we would use to defibrillate, and try to figure out ways to get the charged defibrillator to turn the shock off. We should already know how to do this.
All that appears to be required is competence. Why is that so difficult?
Why do we keep making excuses for misbehavior?
 CPR Before Defibrillation
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Rhythm-Based Management of Cardiac Arrest
Free Full Text from Circulation with links to Free Full Text PDF
 Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study.
Edelson DP, Robertson-Dick BJ, Yuen TC, Eilevstjønn J, Walsh D, Bareis CJ, Vanden Hoek TL, Abella BS.
Resuscitation. 2010 Nov;81(11):1521-6.
PMID: 20807672 [PubMed - indexed for MEDLINE]
Yesterday I described the problems with the recent article claiming that corruption was the reason the AHA (American Heart Association) recommended AEDs (Automated External Defibrillators) be placed in non-acute care parts of hospitals. Today I will look at the study that seems to have inspired the article, even though it came out a year ago.
Does the research claim that there is any suspicion of corruption in the recommendation?
No. The corruption claims appear to be entirely due to the ideological bias of this conspiracy theory site.
Although some studies have shown that AEDs improve survival for out-of-hospital cardiac arrests occurring in certain public locations in which 45% to 71% of cases are treatable with defibrillation,5,6,7 these devices may be less effective or potentially harmful when used in hospitals where only 1 in 5 hospitalized patients have initial cardiac arrest rhythms that respond to defibrillation.8 
Is it wrong to look at the research and recommend that the AEDs be used in settings where a manual difibrillator is not available?
The difference between a manual defibrillator and an AED is that the AED will interpret the heart rhythm itself. The nurses and doctors do not need to be able to do this. This makes AEDs ideal for public places where non-medical people can use them to shock a patient out of a fatal heart rhythm. In those settings, AEDs probably save thousands of lives each year.
With a manual defibrillator, there is much greater cost for equipment and for training to be able to identify shockable rhythms. In the hands of someone familiar with resuscitation a manual defibrillator can be used to deliver a shock with only a few seconds of interruption in compressions, while the AED requires almost a minute of interruption. The greatest problem with resuscitation may be interruptions in compressions., 
What were the results of the study?
The big benefit from an AED would be when a shockable rhythm is the cause of a cardiac arrest in a less than acute care setting. The nurses are not likely to be certified in ACLS (Advanced Cardiac Life Support). The doctors probably have not treated a cardiac arrest since their last ACLS class. There are no manual defibrillators in that part of the hospital.
While the use of AEDs would require longer interruptions of CPR for the AED to analyze the rhythm, one expectation would be that there would be a significant increase in successful resuscitations of patients with shockable rhythms. According to the data above, only about 1/5 of patients who had the AED applied actually had shockable rhythms ventricular fibrillation of pulseless ventricular tachycardia.
The patients were very well matched for everything that might predispose toward a survival advantage in either group.
Even worse is that the anticipated significant increase in resuscitation of patients with shockable rhythms did not happen.
The good news is that hospitals seem to be doing a great job of defibrillating patients quickly without the AEDs.
The median time to shock is 2 minutes. That is recognizing a pulseless, apneic, unresponsive patient, calling a code, beginning CPR, and getting the defibrillator to the patient, turning it on, and delivering shocks to appropriate patients.
The message from this study appears to be that the hospitals are not experiencing significant delays in delivering shocks without AEDs, so there is not likely to be any benefit from adding AEDs. The possible worsening of outcomes is probably due to complicating the response to resuscitation.
Hospitals are big buildings with a lot of people. Many of these people will experience cardiac arrest. Those are two of the things that suggest that AEDs would improve outcomes.
There is an important difference between hospitals and casinos, airports, and other buildings that showed dramatic increases in survival from cardiac arrest after the addition of AEDs and the training of staff in the use of AEDs.
I started out by asking, Is it wrong to look at the research and recommend that the AEDs be used in settings where a manual difibrillator is not available?
Hospitals already have plenty of manual defibrillators and staff trained to use the defibrillators. While there may be many ways to improve the responses in hospitals, the addition of AEDs does not appear to improve responses to cardiac arrest.
Should the AHA have made this recommendation? The AHA too often goes from no recommendation to permanent part of the treatment guidelines without any transitional phases for assessment of benefits. Their reasoning is understandable. What if this is a treatment that will save thousands, or tens of thousands, of lives? Do we want to delay such a wonderful treatment. Part of me still expects to see the ACLS guidelines printed by Acme.
As with second marriages, the AHA seems to continually expect optimism to triumph over experience. The AHA needs to be more cautious.
It is too easy to implement a plan and too difficult to reverse course. How many of the AHA guidelines worked out as planned? Are we really going to miss out on the next multi-thousand patient life saver? If we don’t play the lottery, are we giving up on a shot at millions? We need to put less emphasis on unproven interventions.
In light of our data, national organizations and hospitals may need to reconsider the use of AEDs in general hospital ward units or develop different strategies for using them.
Maybe hospitals should donate/sell their AEDs to places/organizations that are more likely to benefit from AEDs. Large buildings, EMS agencies, fire departments, police departments, et cetera.
 Automated external defibrillators and survival after in-hospital cardiac arrest.
Chan PS, Krumholz HM, Spertus JA, Jones PG, Cram P, Berg RA, Peberdy MA, Nadkarni V, Mancini ME, Nallamothu BK; American Heart Association National Registry of Cardiopulmonary Resuscitation (NRCPR) Investigators.
JAMA. 2010 Nov 17;304(19):2129-36. Epub 2010 Nov 15.
PMID: 21078809 [PubMed - indexed for MEDLINE]
This post can also be found at 510 Medic.
It’s no secret that I’m a fan of capnography. One of the reasons I started a blog was to pass on what I felt were the best practices in EMS. Really that’s a huge part of the EMS 2.0 movement. So let me just say again, for the record, that capnography absolutely qualifies as a “best practice” and may be one of the greatest tools added to our arsenal in my time in the field. Though not universal, many EMS systems are now utilizing waveform capnography for confirmation of advanced airway placement in cardiac arrest patients. But what else can capnography do? Really, the question should be, what can’t it do?
Most providers are aware that higher capnography readings during a resuscitation are associated with a pending return of spontaneous circulation. But is this true for all patients? In a study published in Critical Care, researchers looked at initial and serial CO2 readings in full arrest patients with both cardiac and respiratory origins . The findings were interesting:
So what does this mean for us? Picture the following scenario:
You arrive on scene of a cardiac arrest first. After assessing the patient and finding no pulse, your partner begins chest compressions and you do one of the following next:
The answer to that question ultimately depends on the cause of the arrest right? A patient in cardiac arrest from primarily cardiac causes is likely to be in VF/pulseless VT (depending, of course, on downtime, bystander CPR and the like) and will benefit from early defibrillation. If a patient is in cardiac arrest from primarily respiratory causes (for instance a choking), they are more likely to need oxygenation. Ultimately, the history of the patient and their current medical condition affects the order of your steps on a call.
Now skip ahead a bit in the call. The next due unit has arrived and you have all the manpower you could possibly need. The patient is intubated and on the ECG monitor (which is showing PEA). Your initial post-intubation EtCO2 reading was 30 mmHg, but it has dwindled over a period of minutes to 15 mmHg. One of the other responders mentions that this might indicate that the resuscitation will be terminated. Is this true? It all depends on the patient’s history. If this was a cardiac arrest of respiratory origin, this may be the expected dip in the EtCO2 before an anticipated rise and, ultimately, a return of spontaneous circulation. If this is a cardiac arrest of primarily cardiac origin, it may well mean that the patient will not regain pulses. The take home lesson in this study is that capnography is really just a tool and findings must be interpreted in conjunction with a thorough history.
The authors cite several limitations to their study including the need for a larger cohort study and the fact the EtCO2 is only an approximation of cardiac output. I’d like to add another one for application of this study to EMS: time frame.
The study found that EtCO2 values in cardiac arrest from both primary cardiac and asphyxial causes reached a prognostic value for ROSC in five minutes. Even in an urban system (with lots of paramedics), I would guess that it is probably unlikely that intubation has been performed with regularity within five minutes of the start of a code, even less likely within the three minutes required to see the drop in EtCO2 for asphyxial arrest. There is a way around this, however. Our crews have had good luck placing the capnography fitting between the BVM and facemask when using a BLS airway. This could allow for collection of capnography readings immediately upon start to run the code. Does anyone else use capnography inline with the BVM and facemask? Any feedback or stories?
 - Weil MH: “Partial pressure of end-tidal carbon dioxide predicts successful cardiopulmonary resuscitation in the field”. Crit Care 2008, 2:90.
 – Lah, K; et. al: “The dynamic pattern of end-tidal carbon dioxide during cardiopulmonary resuscitation – difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest”.Crit Care 2011, 15:R13.
Check this out…
Section of Pediatric Surgery, Department of Surgery, The University of Michigan Medical School and The C.S. Mott Children’s Hospital, Ann Arbor, MI 48109, USA.
BACKGROUND: Guidelines for termination of resuscitation in prehospital traumatic cardiopulmonary arrest (TCPA) have recently been published for adults. Clinical criteria for termination of care include absent pulse, unorganized electrocardiogram (ECG), fixed pupils (all at the scene), and cardiopulmonary resuscitation (CPR) greater than 15 minutes. The goal of this study was to evaluate these guidelines in a pediatric trauma population.
METHODS: Pediatric trauma patients with documented arrest were included in the study. Data assessed were duration of CPR, ECG rhythm, pulse assessment, pupil response, transport times, and standard injury criteria (eg, mechanism of injury). Survivors were compared to nonsurvivors using descriptive statistics, chi(2), and Pearson correlation.
RESULTS: Between 2000 and 2009, 30 patients were identified as having had a TCPA. Of the 30 with a prehospital TCPA, there were 9 females and 21 males (0.2-18 years old). The average (SD) injury severity score was 35.4 (20.6). Twenty-four patients (80%) did not survive. Severe traumatic brain injury was associated with nonsurvivors in 78%. One-way analysis of variances demonstrated that CPR greater than 15 minutes (P = .011) and fixed pupils (P = .022) were significant variables to distinguish between survivors and nonsurvivors, whereas ECG rhythm (P = .34) and absent pulse (P = .056) did not, 42 +/- 28 minutes for nonsurvivors and 7 +/- 3 minutes for survivors.
CONCLUSION: Criteria for termination of resuscitation correctly predicted 100% of those who died when all the criteria were met. More importantly, no survivors would have had resuscitation stopped. Duration of CPR seems to be a strong predictor of mortality in this study.
Whether your patient is an adult or a child, transporting them without a pulse is senseless. ACLS treatment for the pulseless patient in the hospital is not much different than in the field. How good will your chest compressions be during transport? We know that good chest compressions is the single most influential factor in cardiac arrest care. The best chance that a dying patient has to regain a pulse is on scene–almost always. It is very difficult to not work a SIDS baby. SIDS has a 100% rate of resulting in death, otherwise it would be an ALTE–apparent life threatening event. I could never judge a colleague for not feeling comfortable with calling a kid on scene. Just keep in mind that you are not doing them any favors by transporting them without a pulse.
An interesting abstract came across Google Reader just now about the prehospital use of hypertonic fluids in patients with traumatic brain injury. Before discussing the results themselves, I’d like to point out one aspect of particular note: The study authors looked at 6 month outcomes. Compare and contrast this to most of the available cardiac arrest research which is only looking at return of spontaneous circulation (ROSC). The authors in this study are clearly thinking further down the road. ROSC in and of itself does not equate to improved patient outcomes. Perhaps we could start looking at resuscitation outcomes 6 month after arrest when publishing new cardiac arrest guidelines, just a thought.
Time for a little review. If you remember, there are three types of solutions used in medicine: Hypotonic, hypertonic and isotonic. Isotonic solutions like 0.9% “normal” saline have the same concentration of solutes (stuff dissolved in them) as the body. Hypotonic solutions have a lower concentration of solute and hypertonic solutions have a greater concentration. What does this mean in the body? Water (the solvent) tends to move to areas which have a higher concentration of solute (solids). This tendency of water to “even out” concentration creates a force called osmotic pressure. When blood cells (as an example) are exposed to solutions with different concentrations of solute the following results are typical:
When the cells are placed in an isotonic solution, nothing changes. The flow of water into the cells is matched by the flow of water out of the cells. When the cells are placed in the hypotonic solution, water flows into the cells to offset the higher concentration inside, causing the cell to swell and break open. And finally, when the cells are placed in the hypertonic solution, water flows out of the cells in an attempt to normalize the solution outside of the cell.
APPLICATION IN MEDICINE
So what does this all mean to medicine? We carry isotonic fluids on our vehicles and routinely use them for fluid resuscitation because we want to increase blood volume without placing unneeded stress on the body’s cells. This study looked at giving a single 250cc bolus of a hypertonic solution to patient with traumatic brain injury (TBI). One of the effects of TBI is swelling of the brain or cerebral edema. The idea of giving a hypertonic solution to a TBI patient makes sense from a chemistry sense; it will keep the fluid from being taken up by the brain tissue because osmotic pressure is keeping the fluid in the blood stream. Basically a hypertonic solution has a tendency to pull water into the blood stream rather than allowing water to leave the blood stream into surrounding tissues. Giving a hypotonic solution to a TBI patient would likely increase cerebral edema.
The authors of the study planned to enroll 2122 subjects who would be given a 250cc bolus of 7.5%saline/6%dextran, 7.5%saline or 0.9% “normal” saline by prehospital providers. The study was terminated after 1331 patients when the study had met “predefined futility criteria”. Not having access to the full article, I’m unaware of what those criteria were. The results, however, show that there was not a statistically significant change in patient outcomes with regard to which fluid bolus was given.
So there you have it. Prehospital administration of hypertonic fluids does not change six month outcomes in TBI patients. Hopefully the chemistry review was worthwhile. If there’s any interest in continuing these types of reviews, let me know and I’d be happy to make it a regular feature. I also think that the study design, and focusing on longer term outcomes is a beneficial approach to prehospital research. At the end of the day, getting pulses back on a cardiac arrest patient doesn’t matter much if they don’t leave the hospital and go on to live a healthy life just like an improvement for a period of hours or days for TBI patient doesn’t mean much if their long term outcome doesn’t improve. What do you think? Are there any other areas of EMS treatment which could benefit from the study of long term outcomes?
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.
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.
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.
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.
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.
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.
One of the benefits of my software engineering job is access to a large corpus of journals through ScienceDirect. About once a month I pick a topic and pull the latest research. This month I did a journal search for “paramedic” AND 2010 which returned many interesting articles. One that particularly piqued my interest was Berdowski J, et al: Delaying a shock after takeover from the automated external defibrillator by paramedics is associated with decreased survival . The authors found that when the paramedics switched from the AED to their monitor and a shock was delayed, for whatever reason, there was a decrease in patient survivability to discharge (ed: original copy did not appear to specify ‘to discharge’, current copy of article clearly states to discharge, updated).
Currently I work for two services in two different counties, one is a BLS industrial fire brigade and the other is an ALS combined Fire/EMS department. Both services have AEDs for their BLS providers with pads that are interchangeable with the monitors predominantly carried by the ALS units in their respective counties (Philips in one, Physio in the other). The standardization on pads obviously makes BLS to ALS patient handoff simpler during cardiac arrest. However, I had not considered at what point in resuscitation would be the most appropriate to make the pad switch.
The research showed that in nearly two thirds of the cases where a switch from the AED to the ALS monitor was made, the delivery of an appropriate shock was delayed. Barring equipment or operator malfunction, an AED and a paramedic are both going to defibrillate the same rhythms. Paramedics can still place the patient on their monitor with a 3-Lead even if they have not changed the pads over. The study authors concluded that the appropriate time to switch the pads would be after the AED delivers a shock or advises that no shock should be delivered.
The mechanics of a patient handoff from a BLS unit to an ALS unit during cardiac arrest are not something touched on in paramedic school or ACLS . The handling of compressions versus defibrillation is rightfully stressed, but this appears to have missed another factor critical to patient survival. In retrospect this factor is obvious and thankfully easily correctable, perhaps simply through recognition. ACLS classes geared towards pre-hospital providers can add this into scenarios used for testing and EMS protocols can include text similar to:
Minimize interruptions in compressions or appropriate defibrillation delivery by first responders when initiating ALS treatments in cardiac arrest.
This minor change is low hanging fruit compared to the benefit to our patients!