Wolff-Parkinson-White (WPW) - STEMI Mimics

Tom B | 12:22 PM | | 2 comments

A really interesting 12-Lead ECG was posted to the Cardiology & Electrocardiography (ECG, EKG) Experts group on Facebook the other day.

If you're not familiar, this is one of the groups / fan pages on Facebook I help moderate with Jason Winter who also started the Cardiology & Electrocardiography Experts blog.

What's so interesting about this ECG is that it shows a relatively infrequent STEMI mimic. In addition, it helps demonstrate a point I've been pondering about several of the STEMI mimics in general.

Let's take a look.



The patient was a 29 year old male with no complaints. The ECG was captured during a routine workup according to the contributor Chris de Beer (thanks again for the interesting ECG, Chris).

The ECG shows a WPW pattern as evidenced by a short PR interval and delta waves. The delta waves create a pseudo-infarct pattern (Q-waves) in the septal leads.

You might recall from my previous post about left ventricular hypertrophy (LVH) that I think recognizing the so-called "strain pattern" is actually more important than knowing the "voltage criteria" for LVH.

I'm sure some of you are waiting for "Part II" of the left ventricular hypertrophy series, but I'm still waiting for inspiration! :)

What does this ECG have in common with a strain pattern from left ventricular hypertrophy (LVH)? What does it have in common with left bundle branch block (LBBB)? What does it have in common with ventricular rhythms? Including paced rhythms?

The answer is, it has a widened QRS-T angle! To put it another way, the T-waves and ST-segments are deflected opposite the main deflection of the QRS complex, and (this point is the most critical) the degree of the ST-T abnormality is proportional to the size of the QRS complex.

Think of this as a supplement to Sgarbossa's criteria and the "rule of appropriate T-wave (and ST-segment) discordance".

Here's a graphic to help illustrate the point.



When you see a pattern like this, regardless of cause, it should set off alarm bells that you are dealing with a STE-mimic and not acute STEMI!

Note that the S-wave in lead V3 is cut off by the bottom of the ECG paper. This is a common problem with prehospital 12-lead ECGs! We must presume that the S-wave would be the deepest in lead V3 if we were able to view the entire QRS complex.

That doesn't mean the patient isn't experiencing acute myocardial infarction (although this patient is asymptomatic so let's pretend he was over the age of 30 and complaining of chest discomfort).

It just means you should wait before pulling the trigger on the cardiac cath lab.

Look for changes on serially obtained ECGs instead!

See also:

Left ventricular hypertrophy

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graphic

ECG mimics of acute STEMI

California Man Dies after Declining EMS

Shaggy | 12:47 AM | | 2 comments

So I just read an article of a man who went to bed and never woke up after an accident where he refused EMS, and many thoughts ran through my head. This guy rolled his vehicle and suffered blunt force trauma to the head. He signed a refusal to EMS, and he was on his merry way. I have many questions. Was he restrained or ejected? What did he strike his head on? Did he lose consciousness? What was his true mental status at time of assessment? Was there a legitimate assessment done? If not, did he refuse even assessment? Was medical command consulted? Why do I ask? This is an unfortunate event that resulted in the untimely death of a very young adult. We have experienced or have potential to experience similar episodes. We need to ensure our patients don't slip through the cracks.

So, whose fault was it that he died? Well, inevitably, it was his own. He had drugs in his system while driving; he lost control of his vehicle, most likely from driving too fast; he was probably not restrained; and most of all, he refused medical treatment. Does that mean he was clearly an idiot? Maybe. Maybe not. Does this absolve the EMS crew of any responsibility? This is where I would like to have some more information to answer that. It could be that the EMS crew may or may not have done all they could have done. Am I discussing liability? I hate discussing liability. I would rather discuss good patient care and the prevention of premature deaths like this young man we are discussing. That should be our driving force. Not tort prevention. Anyway, that is neither here nor there. What I want to discuss is how can WE try to prevent an episode like this from occurring on one of OUR calls.

I asked about MOI. Rollovers are no longer criteria for trauma center transports since last year, though many systems still advocate it. However, with a rollover, more investigation needs to be done to determine the MOI directly to the patient. Did the vehicle flip multiple times? Was he unrestrained and hit he his head against the windshield or damage the interior of the vehicle with his body? The MOI is not a guidance to treatment nor mode of transport but the MOI may determine the appropriate destination hospital, such as LVL1 or LVL2 trauma center. It does not indicate need for helicopter. Distance to trauma center AND assessment findings do. It DOES mean you need to be more suspicious and focus your assessment on that suspicion, based upon the MOI. In this case, a complete trauma assessment, ensuring to pay particular attention on the head with a good neuro exam.


http://www.coraopolisvfd.com/photo_gall.htm
Someone at face value may appear benign, but upon closer evaluation, may show subtle signs or symptoms of a serious injury. So for this reason, we should not be so lax when responding to these calls even when finding the patient outside the vehicle visibly appearing uninjured. I know most of us, myself included, were quick to get a refusal in the middle of the night when our sleep was interrupted by some bozo who wrecked his or her car, and is found outside giving police information. I cannot emphasize enough the importance of doing a thorough assessment based upon the MOI, and this is a good case of why!

www.flickr.com/photos/nomadmedic/3792340425/


Let's say an assessment was performed and the assessment appeared unremarkable. With a MOI that caused blunt force trauma to the head, he should still be advised that further medical evaluation is necessary. Don't just tell him that. Patients will just tone that out. Explain WHY he should be evaluated at a hospital. Explain the process of TBIs in how their effects are not often readily evident and how people wake up, or, well, don't wake up-dead. Explain about forces that can damage internal organs like major blood vessels that can again, take time to manifest signs and symptoms. You may also want to get medical command to speak to him to explain the risks of not going to the hospital. If after all of that, he refuses ambulance transfer for whatever reason, try to get his assurance that he will seek evaluation at an ED ASAP. There have been many patients that I have evaluated who did not appear to NEED an ambulance, but should get further medical evaluation and treatment, who I felt easy allowing them to go by POV to the hospital. We all have. This guy, if he went by POV directly to the hospital, and got scanned, he may be alive today, although, I would advocate ambulance transport for him. ED MDs seem to give more attention to the patient brought in by ambulance than POV. If he refused to even go the hospital on his own, give him a list of signs and symptoms to be vigilant for as well as their significance. Of course you will instruct to call EMS or seek an ED if these signs and symptoms develop.


Now let's say further assessment WAS remarkable. You observe abnormal findings and realize he NEEDS to go to a trauma center. He refuses. You give him the speech and try to educate him. He still refuses. Now what? This is where it is imperative to get a hold of medical command and get the MD to speak to him. If he STILL refuses, you are pretty much legally off the hook. Otherwise, you would have to force him against his will, and they you are tempting kidnapping charges and violating patient autonomy. But you still have an an option or two. If police are present, try to use their authoritative demeanor to try and convince him. Of course, if the patient's condition does appear serious enough, there is also the option of taking him involuntarily, but only after medical command consultation. Otherwise, if you go that route, you better be prepared to justify it. The police will not usually get involved if the patient shows no altered mentation and unless you can can show it was obvious the patient would surely and quickly die otherwise, you may be asking to be sued. Therefore, I advocate to stay away from the notion of kidnapping. IF after all is said and done, and he still refuses, beg him to go on his own to the hospital, primarily a trauma center, and explain to him why.

Be sure to document well no only the scene survey and assessment results, but also ensure you state in detail all of your efforts to convince the patient to be transported to the hospital. Many states or agencies have their own special refusal forms, with a copy that goes to the patient. Ensure this is completed well, and if your narrative section is small on the refusal form, ensure your efforts to convince the patient are listed there. Ideally this info should be on the form signed by the patient and the copy given to the patient that lists your efforts. Attorney (and paramedic) W. Ann Maggiore advocates for a multi-tiered patient refusal form that applies to different types of contacts, such as the patient who needs to go but refuses, the patient who should be seen but does not necessarily need EMS and the person who does not become a patient at all, such as the fender bender you are routinely called to by bystanders but all parties involved are just trying to exchange insurance info and are denying injuries.

I know this goes without saying, but please don't deviate from your refusal protocols. The courts generally adhere to the concept of patient autonomy, and if the patient refuses, your adherence to your protocols and proper documentation are what will protect you legally when the patient or family try to sue you later, such as in this case.

So to summarize, the concepts are do a good scene survey to evaluate MOI to determine how to focus your assessment and appropriate destination hospital. We do an appropriate assessment based upon the MOI. Not a half-assed one. Those are the ones that burn us. Explain the risks, not just in vague terms, but really explain them. And get medical command involved if necessary. Just getting a signiture on a refusal form is not enough. So when you go home at the end of your shift, and you learn the patient who refused later turned up dead, your conscience should could be clear you gave your best effort for what was best for the patient. Then you can say for sure if he was really an idiot or not.

Just some interesting related literature:
Stacey Knight MStat, Lenora M. Olson MA, Lawrence J. Cook MStata, N. Clay Mann PhD, MS, Howard M. Corneli MD and J. Michael Dean MD, MBA, Against all advice: An analysis of out-of-hospital refusals of care, Annals of Emergency Medicine, Volume 42, Issue 5, November 2003, Pages 689-696

S.Mulholland, B.Gabbe, P.Cameron, Is paramedic judgement useful in prehospital trauma triage? Injury, Volume 36, Issue 11, Pages 1298-1305

Robert P. Pringle, Jr MD, Donna L. Carden MD, Feng Xiao MD and Derrel D. Graham, Jr MD, Outcomes of patients not transported after calling 911, Journal of Emergency Medicine Volume 28, Issue 4, May 2005, Pages 449-454

Lynn K. Wittwer, MD, MPD, Refusal of Medical Assistance, slide presentation

Interview with Keith Lurie, M.D. discussing the ResQPOD and the ROC PRIMED trial

Tom B | 9:53 AM | | 4 comments


Keith Lurie, M.D.
Co-Director, Cardiac Arrhythmia Center, Central Minnesota Heart Center, St. Cloud, MN
Staff Cardiologist, St. Cloud Hospital
Professor of Internal and Emergency Medicine, University of Minnesota
Chief Medical Officer, Advanced Circulatory Systems


Dr. Lurie – thank you for this opportunity to discuss impedance threshold device technology and the ROC PRIMED study.

I see that you attended Stanford School of Medicine. Where did you complete your undergraduate degree?

Yale University

Did you enjoy medical school?

Very much so. I could not afford to go without working and I worked 20 hours/week in a lab to pay my way. I was exposed to some fantastic teachers and became a researcher in the process.

Why did you choose Cardiology?

I worked in med school in a lab that did heart transplant research. I became interested in the biochemistry and pharmacology of the heart, did lots of heart transplants in animals, and became fascinated by the complexity and beauty of the cardiovascular system. I also like to do procedures so it was a natural.

You did your residency at the University of Pennsylvania and a fellowship at the University of California – San Francisco. Could you briefly explain to my readers the difference between a residency and a fellowship?

During residency you learn how to become a doctor and during a fellowship you narrow down to a specialty or subspecialty area. So during residency I became an internal medicine doctor (instead of, for example, a surgeon). During my fellowship I became a cardiologist and then later a cardiac electrophysiologist.

How did you end up at the University of Minnesota?

I wanted to stay in academic medicine, the U of Minnesota had an excellent program, and my sister and brother-in-law both were academic docs at the U of Minnesota. My wife and I loved San Francisco but it was a difficult place to raise a family and have an academic career. We have been very happy in Minnesota.

You’re also an inventor, the holder of several patents, and the founder of a company. Did you always see yourself as an inventor and an entrepreneur?

In college I never thought about becoming an inventor and I never wanted to become a businessman. I studied architecture and discovered I had some creativity but decided to go to medical school as I also loved biology. In 1990 I reported in JAMA on the use of a toilet plunger by family members who performed CPR on their dad with a household plunger (CPR: the P Stands for Plumbers Helper). A colleague told me I should patent the idea. I told him I knew nothing about patents but if he wanted to enlighten me I was game. Twenty years later I know a lot more about this process.

I started Advanced Circulatory Systems Inc in 1997 against my better judgment as I really did not want to become a businessman. However, while studying the plunger idea we discovered the idea of an impedance threshold device (ITD) and no other medical device company was interested in the ITD concept we discovered at the U of Minnesota. Every time we tested the ITD in pigs during CPR is was pretty amazing. Blood flow to the heart and brain was 4x higher with the ITD and active compression decompression (ACD) CPR (plunger CPR) compared with manual standard CPR and 2x higher with the ITD and standard CPR vs standard CPR alone.

Ultimately I realized I could write lots of papers but not necessarily impact patient care through research. Alternatively I could potentially start a company to get this technology out into clinical use and maybe help make a bigger difference. It has been a long journey, with some very high points and a few low points. One very high point was when the plunger device, (the CardioPump) and the ITD were used together on our 2007 U of Minnesota cardiac electrophysiology fellow after he had an out-of-hospital cardiac arrest while jogging in Minneapolis 1 month after he finished his EP training. He survived, was also treated with therapeutic hypothermia, and practices EP today! That was clearly a high point.

How did you come up with the idea for the ResQPOD (Impedance Threshold Device or ITD)?


I was bothered by the fact that there were disparities in the benefits associated with active compression decompression (ACD) CPR (CardioPump) and I was studying it in an acute model of VF. Patients in need of an implantable defibrillator (ICD) in 1991 had a new option to get a device with a pacer-like lead placed in their heart. Prior to that time when you needed an ICD the chest was opened with a thoracotomy and electrode patches were placed on the heart. With the new transvenous approach, the one we use today where the leads goes through a vein into the heart, the FDA made us induce VF successive times until we found the defibrillation threshold. This means that at least one time the ICD would always fail and then we needed it to recharge and defibrillate the patients with a higher amount of energy. Sometimes we had to do manual CPR and after that happened a couple of times I decided to compare the acute physiology of VF during manual standard CPR versus ACD CPR.

We obtained IRB approval and conducted a little study. With ACD CPR minute ventilation was 16 L/min vs 4L/min with standard CPR. Coronary perfusion, ETCO2, and systemic blood pressures were about 25% higher with the ACD CPR. However, we were also measuring the pressure inside the thorax with an esophageal manometer and there was no difference between standard CPR and ACD CPR. That bothered me. I was talking to a colleagues, Mike Sweeney, an anesthesiologist, about this and told him I did not know why the intrathoracic pressure was not going down each time we pulled the chest upward with the ACD CPR device. He suggested that we pre-oxygenate the next patient we operated on and when I did ACD CPR he would occlude the ET tube with his thumb. The first time he did this we watched the esophageal manometer pressure plummet to -10 mmHg when I pulled up with the ACD CPR device and I knew immediately that we had discovered something. It was a Eureka moment. By preventing air from rushing into the lungs, we created a greater negative vacuum and that sucked more blood back to the heart.

Within 6 months we published an article in Circulation showing that when performing ACD CPR in pigs, transiently preventing air from rushing into the lungs during the decompression phase (chest wall recoil) of CPR with a one way valve would result in a lower intrathoracic pressure. The lower intrathoracic pressure causes more blood to move back into the heart, refilling it better for the next time the chest is compressed. We showed that you could normalize blood flow to the brain with this approach (compared with 20% of normal blood flow with manual CPR) and provide the heart with 70% of its normal blood flow. We later modified the ITD so that if a patient woke up they could breathe through it and we added a timing light to guide the ventilation rate (1 quick breath per flash) and the compression rate (10 compressions between flashes). It was ~ 10 years later when we rediscovered that lower intrathoracic pressures cause lower intracranial pressures immediately, and thus one of the additional reasons brain flow was normal in these pigs getting ACD CPR and the ITD.

How exactly does the device work?

The device is mechanically relatively straightforward but physiologically more complex.

When you compress the chest air leave the lungs through the ITD with minimal or no impedance. When you ventilate a patient during CPR air goes into the patient through the ITD with minimal or no impedance. However, when the chest is recoiling (passively or actively) after being compressed, the ITD blocks air from entering the lungs, thereby creating a greater decompression phase vacuum inside the thorax. This pulls more blood back into the heart and lowers intracranial pressure. In this way the heart is more efficiently refilled after it is emptied during the compression phase and the brain gets more blood by two different mechanisms. If the patient starts to breathe after they are resuscitated, they can breathe through the ITD but it can be difficult.

The ResQPOD that is being sold commercially in the US has -10 cm H2O resistance when a patient inspires through it. The ITD used in the ROC study had a -16 cm H2O resistance. The higher resistance is needed to optimize ACD CPR (which we thought would eventually be used in the US at it is used now in some other countries). However, with standard CPR we never achieve a very large vacuum in the thorax with passive chest wall recoil so -10 cm H2O resistance is adequate. That is, with passive recoil of the chest, the vacuum created with an ITD is typically only -2 to -6 cm H2O.

So, in short, the ITD turbo-charges CPR. It doubles blood flow back to the heart when used with manual standard CPR and it lowers intracranial pressures (ICP) (part of the normal physiology we rediscovered about 8 years ago). This results in more blood flow to the brain as there is less resistance to forward flow.

You have to take the ResQPOD or ITD off of the patient when not doing CPR or it can cause potential harm after the patient has been resuscitated. On the other hand if a patient is gasping but in cardiac arrest then they are trying to generate a negative intrathoracic pressure on their own and you should leave the ResQPOD on the patient as long as CPR is needed and being performed.

Most people do not know that each time we take a breath and inspire spontaneously, or when we create a negative intrathoracic pressure within the chest during the decompression phase of CPR with the ITD, this lowers intrathoracic pressure and the lower pressure in the thorax is immediately transferred to the brain via the rich venous plexus surrounding the spinal cord. So with greater negative intrathoracic pressure, the ICP goes down.

Thus, we can lower ICP by lowering intrathoracic pressure. One way to do this is with the ITD or ResQPOD. Needless to say we did not rediscover this overnight but we believe this is contributes to why more patients wake up after cardiac arrest when they are treated with the ITD. The lower the ICP or resistance to forward blood flow, the more blood will go to the brain. This principle has not been well exploited in medicine. The converse is also true. One of the reasons that pressure bombs cause head injury is that pressure waves are transmitted through the abdomen and thorax via the spinal cord and venous plexus around the cords to the brain and this can cause a sharp and deadly rise in ICP.

The device was given a Class IIa rating in the 2005 AHA ECC guidelines, which is higher than any medication. Were you excited about that?

A double-blinded randomized study by Drs Parrillo and Aufderheide in 2004 made 3 fundamental new observations:
  1. Hyperventilation during CPR was common and later shown in pigs to be deadly
  2. Incomplete chest wall recoil during CPR because people lean on the chest is common and was shown later in pigs to be very harmful
  3. The ITD doubled blood pressure during CPR.

That study along with other studies in animals and people convinced us to launch the product in the US. The study results were exciting. The AHA recommendation of Class IIa based upon increased circulation has helped get this technology out onto the streets and helped to save lives. Some of the largest EMS systems in the country are have implemented all of the Class I and IIa recommendations including the ResQPOD. Fewer people are dying in those cities after cardiac arrest now and that is very gratifying.

I think many of us who have been following the ResQPOD were surprised by the recent announcement by the National Institute of Health that the ROC PRIMED trial was stopping enrollment.

Tom Aufderheide, MD was quoted as saying, “While the ITD is based on sound physiologic principle, in this study it did not appear to improve survival rates for adults in cardiac arrest outside the hospital.”

Considering that the ROC PRIMED trial was a prospective, multi-centered, randomized clinical trial with large enrollment, are you concerned about these results?

I think it is important to begin my response by saying that we do not know all of the results of this trial; all we know is that if they had continued it that the results would not have been conclusive. I also know that if you ask Dr. Tom Aufderheide “would you want the ITD used on your mother if she went into cardiac arrest” he would say something like, “yes, as long as she was also receiving high quality CPR with good chest compressions.”

We know that complete study results will not be disclosed for 6 - 12 months. What we know is from discussions with key personnel involved with the study and from press statements. So to directly answer your question, I am not concerned with the results, nor am I surprised.

I feel it is important to focus on the lessons learned already from the ROC study so that we can improve outcomes uniformly when rescue personnel use the ITD. As the founder of the company that makes the ITD, I continue to believe in the fundamental physiology underlying the ITD, its potential to increase circulation in patients in cardiac arrest, and in the potential for the ITD to increase neurologically-intact survival rates, especially when the device is used in emergency medical services (EMS) systems that are already performing well.

Let me explain a bit about the study results. There were four key findings that we know so far:
  1. There were no safety issues with the ITD.
  2. Some sites saw a benefit with the active ITD and others did not; on average no increase in neurologically-intact survival to hospital discharge benefit was observed.
  3. Overall survival rates increased during the study compared to baseline.
  4. The study arms that concurrently evaluated 30 seconds of CPR versus 3 minutes of CPR followed by analyze and shock found that both groups had similar outcomes.

I also know from confidential discussions that the cities that had the highest survival rates before the ROC PRIMED study had an increase in survival rate with the active ITD compared with the sham during the this study.

Do you expect that the ResQPOD (Impedance Threshold Device or ITD) will be downgraded to a Class IIb rating in 2010?

While I am not involved in that process, and was not previously, the AHA committees that make that determination will look at all of the data available this year. The ROC ITD study was neutral and I believe that the ITD will continue to have a Class 2a recommendation. One study with over 1000 patients published by Aufderheide et al in 2009 showed a significant increase in survival rates compared with historical controls in 6 large EMS systems (Crit Care Med 2008; 36[Suppl.]:S397–S404). There was a >50% increase in survival for patients presenting with ventricular fibrillation. Another recent study comparing in-hospital ITD use with historical controls showed a 65% increase in neurologically-intact survival to hospital discharge for patients treated with the ITD: the historical controls had a 17% survival to discharge versus 28% in the ITD-treated group. (Thigpen et al, J. of Respiratory Care, in press, 2010). So far all of the studies have been positive and the ROC study overall was neutral. I believe there will be some subgroups even in the ROC study will show a strong trend towards a benefit.

In the study design, patients were randomized to one of two devices: the “active” ITD or the “sham” ITD. Did both devices look identical to the rescuers and were both equipped with a timing light for ventilations?

Yes, the devices were opaque and yellow and could not be distinguished when looking at them or feeling them. Both had timing lights that flashed 10x/min.

Do you think the simple fact that patients were not hyperventilated was an important factor in the relatively high survival rates seen in the study?

I am not sure I would agree with your conclusion that there was a relatively high survival rate. Before the study the survival rates to hospital discharge with good neurological function ranged from a low of 1.1% in Birmingham AL to 8.1% in Seattle. The mean neurologically-intact survival rate was 5% in all of the sites during the study: that is close to the national average and not very high at all. I am certain that performing CPR at the correct ventilation rate helped to some degree, but it is hard to know how much. I think both groups were likely to have had a very similar ventilation rate.

Editor's note: This question was based in part on Lisa' Bell's blog post Unexpected Increase in Survival Rates in ROC Study at JEMS Connect.

The study also randomized patients to an “early shock” or a “late shock”. Could you please explain the difference in these two approaches?

Half the patients were treated with 30 seconds of CPR followed by analysis and shock and the other half had 3 minutes of CPR followed by analysis and shock. If the patients still required CPR then it was continued with either an active or sham ITD. In some cases the ITDs were added in the 3 minutes of CPR, analyze, shock group, but usually the ITD was added after these 2 different CPR/analyze/shock interventions. This makes analysis of the ITD effect more challenging to say the least. We know that in many cases it takes longer to get an AED onto a patient so the 30 seconds was more often closer to 60 seconds. We know that the study did not show a difference in outcomes when comparing 30 seconds vs 3 minutes of CPR.

I noticed that even the “early shock” patients received some chest compressions prior to the first defibrillation attempt. Does this study demonstrate that boosting the heart’s perfusion pressure prior to a defibrillation attempt is a critical intervention?

We do not have a control group in this study to draw that conclusion. I can say that one site, Seattle, believed so strongly in CPR before shock for any patient in cardiac arrest >4 minutes before being able to deliver a shock that they refused to participate in the 30 sec vs 3 min of CPR analyze and shock portion of the study. This is also the site with the highest survival rate before starting the ROC PRIMED study.

Is there anything else you’d like to say to about the ROC PRIMED trial, cardiac arrest, or any of your inventions?

I do have more I would like to say and I apologize as it is quite lengthy. But let me premise my comments by saying there is no silver bullet in CPR and we have been foolish for decades to think there is or was. Survival from cardiac arrest requires multiple therapies, just like any other complex disease whether it is heart failure, leukemia, or AIDS. What we strongly recommend is a systems-based approach, where all of the AHA Class I and IIa recommendations are deployed sequentially. We have described this in a program called Take Heart America. With this approach we have doubled survival rates in multiple cities.

My additional comments about the ROC PRIMED study are below.

There were many reasons for the overall neutral results, recognizing that full details will not be available for months. They include:
  1. Multiple study protocols were executed simultaneously:
    1. 30 secs vs 3 mins of CPR analyze shock during BLS for all patients
    2. Three fundamentally different BLS protocols, which included a) following the 2005 American Heart Association (AHA) Guidelines 30:2 protocol, b) continuous chest compressions without interruption for ventilation with a breath every 10 compressions with the 30 seconds vs 3 minutes of CPR, analyze, shock protocol, and c) continuous chest compressions without interruption for ventilation with a breath every 10 compressions without the 30 seconds vs 3 minutes of CPR, analyze, shock protocol.
    3. CPR devices to assess depth of compression and compression rate were tested in some sites
    4. Prehospital cooling was used in some sites
    5. Post-resuscitation care varied greatly
  2. Quality of CPR – variable from site to site, reflected in part by the baseline differences in neurologically-intact survival from 1.1% to 8.1%.
  3. ITD put on late due to the analyze early vs analyze late protocol; on average the ITD was placed ~4 minutes after the start of CPR, often much later.
  4. Potential interactions between analyze early vs analyze late protocol, as CPR was started and stopped prior to ITD placement are unknown.
  5. The ITD was not always removed post ROSC, which can be harmful with the -16 cmH2O cracking pressure in the ROC ITD.
  6. There were very poor survival rates, as low as 1.1% at baseline in some sites, so an effect can be hard to detect even with tens of thousands of patients.
  7. Overall survival rates increased during the study compared with historical, likely due, in part, to a Hawthorne effect that included increased focus on CPR quality. This further limits the statistical ability to show a difference between the active and sham group
  8. Chest compression depth varied from patient to patient and some sites did not emphasize the basics of CPR – that it compress the chest ASAP 1.5-2 inches with minimal compressions. Without good compressions the ITD, which functions like a turbocharger during CPR, is ineffective. There was no mandatory training program or retraining program so that too varied from site to site.
So what are the lessons we learned?
  1. When using the ResQPOD you need to continue to perform high quality CPR; it is fundamental to success. Emphasis on correct compression depth and rate needs to be re-emphasized while at the same time the importance of full chest wall recoil is stressed. In addition, rescuers need to follow the directions for use related to the timing of ResQPOD placement and removal. Training and regular retraining with hands-on, I believe every 3-6 months, is important.
  2. Best results are achieved with a systems-based approach which includes the practice of all of the key AHA 2005 Guidelines. The key guideline recommendations and their class level of recommendation are below.
  3. Early application of the ResQPOD is essential. It should be placed as soon as possible, but after chest compressions are initiated. Chest compressions should always be started right away. Focusing on quality of CPR (it is hard to do and regular retraining is essential) and tracking outcomes are essential to deriving value from CPR in general and from the ResQPOD.

I believe we are on the threshold for a new era in CPR. The kinds of studies that ROC has performed are going to have to change so that systems-based approaches are used otherwise ROC will continue to have neutral or negative studies. Co-variables related to care outside and inside the hospital are too critical to go uncontrolled in the future. These uncontrolled variables impact the integrity of care and study outcomes.

Once we deploy what we know works correctly in systems that function well initially (systems with a 1% survival should never be ROC study sites), we will see even more progress. Ultimately we will also want to regularly deploy automated CPR devices and new techniques that optimize circulation during CPR, (including a device that generates a continuous negative intrathoracic pressure between each intermittent positive pressure breath), perhaps cooling during CPR for patients still in cardiac arrest, and post-resuscitation care that includes cooling ASAP.

I noticed during my research for this interview that NASA inducted the ResQPOD into the Space Foundation Technology Hall of Fame. How did that come about and why does NASA carry the ResQPOD on the Space Shuttle?

In 1998 we started working with NASA and the US Army using the ITD in spontaneously breathing volunteers. Breathing through an ITD with a resistance of only -7 cm H2O, through a device called the ResQGard, lowers intrathoracic pressures, enhances blood flow back to the heart, and lowers ICP. We tested this in many human volunteers, including hypotensive volunteers. This other version of the ITD called the ResQGard is part of the standard care NASA astronauts get if they are hypotensive after prolonged space flight. Upon return to earth it takes a while for their bodies to get used to gravity and they often have severe orthostatic hypotension. The ResQGard helps maintain higher blood pressure and cerebral perfusion. The ResQGard is now being used by EMS systems to treat spontaneously breathing hypotensive patients and it is being used by military personnel to treat hypotensive soldiers. Research on the ITD has been funded by the NIH, the Defense Department, and by NASA. The ITD was inducted into the Hall of Fame as a result of this research. I am not aware that the ResQPOD is being used on the Space Shuttle although it should work in space.

Thank you for this opportunity to share my thoughts with you and your readers.

Helpful links:

ResQPOD Product Animation

ResQPOD demonstration video - pig in cardiac arrest

Rebroadcast of 11/12/09 webinar: Improving Resuscitation with a Systems Based Approach: An Update on Six Clinical Investigations by Keith Lurie MD and Charles Dick MD

Cardiac Arrest Trial Cut Short

NHLBI Stops Enrollment in Study on Resuscitation Methods for Cardiac Arrest

Resuscitation Outcomes Consortium (ROC) PRIMED cardiac arrest trial methods part 1: rationale and methodology for the impedance threshold device (ITD) protocol.

Resuscitation Outcomes Consortium (ROC) PRIMED Cardiac Arrest Trial Methods Part 2: Rationale and Methodology for "Analyze Later" Protocol

Study Compares Passive Oxygen Insufflation and BVM

"New" LBBB - What's the big deal?

Tom B | 11:13 AM | | 0 comments

Cross-posted to the Prehospital 12-Lead ECG blog and 12-Lead ECG (Cardiography & Electrocardiography Experts)

In the January 2010 EMCast at EMedHome.com, Amal Mattu MD reviews Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27:916-921.

His comments confirm what I have suspected for a long time with regard to LBBB in the setting of suspected ACS.

"This is a really interesting and provocative article that may bust the traditional myth that we should be thrombolysing or cathing everybody with chest pain who presents with a new left bundle branch block."

"They found that there was no significant difference in the rate of acute myocardial infarction between patients that were presenting with a new, or presumed new left bundle branch block pattern versus patients with a known old left bundle branch block pattern […] In other words, when patients presented with a new left bundle branch pattern, those patients did not rule-in at any greater increased frequency compared to the other patients, and based on this data the argument is certainly made that when patients have chest pain and they present with the left bundle branch block pattern, there’s not necessary a need purely based on the presence of a new left bundle to assume that that patient is having an acute MI, and therefore that patient needs to get thrombolytics or go immediately to the cath lab."

"As I mentioned before, there is reasonable data to indicate that if the patient has a left bundle branch block – whether it’s new or old – and they demonstrate Sgarbossa criteria, then those patients do end up ruling-in for acute myocardial infarction […] Simple presence of a new left bundle branch block pattern does not appear to warrant immediate activation of the cath lab or immediate thrombolytics according to this study."

Amal Mattu MD does add the caveat that the guidelines still state that patients with new LBBB are supposed to get reperfusion therapy.

See also:

Identifying AMI in the presence of LBBB

False positive cardiac cath lab activations

Review of Factors Associated With False-Positive Emergency Medical Services Triage for Percutaneous Coronary Intervention

Sgarbossa's criteria - new graph

Prehospital Research

Adam Thompson, EMT-P | 11:39 AM | , , , , | 3 comments



Every once in a while I will head over to Pubmed.com and run a quick search on prehospital. It is a good way to stay current in this ever-changing field. It is also good practice to stay relevant when advocating evidence-based medicine. Here are some abstracts from my most recent query. All are open for discussion, so please leave your comments.



Can medics do math?
Pubmed [1]
BACKGROUND: The ability to perform drug calculations accurately is imperative to patient safety. Research into paramedics' drug calculation abilities was first published in 2000 and for nurses' abilities the research dates back to the late 1930s. Yet, there have been no studies investigating an undergraduate paramedic student's ability to perform drug or basic mathematical calculations. The objective of this study was to review the literature and determine the ability of undergraduate and qualified paramedics to perform drug calculations. METHODS: A search of the prehospital-related electronic databases was undertaken using the Ovid and EMBASE systems available through the Monash University Library. Databases searched included the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, CINAHL, JSTOR, EMBASE and Google Scholar, from their beginning until the end of August 2009. We reviewed references from articles retrieved. RESULTS: The electronic database search located 1,154 articles for review. Six additional articles were identified from reference lists of retrieved articles. Of these, 59 were considered relevant. After reviewing the 59 articles only three met the inclusion criteria. All articles noted some level of mathematical deficiencies amongst their subjects. CONCLUSIONS: This study identified only three articles. Results from these limited studies indicate a significant lack of mathematical proficiency amongst the paramedics sampled. A need exists to identify if undergraduate paramedic students are capable of performing the required drug calculations in a non-clinical setting.


Intubation in trauma patients.

Rogue Medic's Airway Post (one of many)
Pubmed [2]
PURPOSE OF REVIEW: The primary purpose of this article is to highlight the latest airway research in multitrauma. RECENT FINDINGS: Management of the airway in multitrauma patients is a critical resuscitation task. Prehospital airway management is difficult with a high risk of failure, complications, or both. In-hospital performed conventional oral intubation with manual in-line stabilization, cricoid pressure, and a backup plan for a surgical airway is still the most efficient and effective approach for early airway control in multitrauma patients. Selective utilization of airway maintenance, instead of ultimate airway control in the field, has been suggested as a primary prehospital strategy. Properties of videolaryngoscopes complement standard laryngoscopes. When compared with a Macintosh laryngoscope, the Airtraq and Airwayscope diminish cervical spine motion during elective orotracheal intubation. Penetrating neck injuries are the most frequent indication for awake intubation, whereas patients with maxillofacial injuries have the highest rate of initial surgical airway. SUMMARY: Risks and benefits of ultimate prehospital airway control is a controversial topic. Utilization of videolaryngoscopes in multitrauma remains open for research. Standardization of training requirements, equipment, and development of prehospital and in-hospital airway algorithms are needed to improve outcomes. Rational utilization of available airway devices, development of new devices, or both may help to promote this goal.


Reduce patient prehospital delay in ACS.
Pubmed [3]
BACKGROUND: Delay from onset of acute coronary syndrome (ACS) symptoms to hospital admission continues to be prolonged. To date, community education campaigns on the topic have had disappointing results. Therefore, we conducted a clinical randomized trial to test whether an intervention tailored specifically for patients with ACS and delivered one-on-one would reduce prehospital delay time. METHODS AND RESULTS: Participants (n=3522) with documented coronary heart disease were randomized to experimental (n=1777) or control (n=1745) groups. Experimental patients received education and counseling about ACS symptoms and actions required. Patients had a mean age of 67+/-11 years, and 68% were male. Over the 2 years of follow-up, 565 patients (16.0%) were admitted to an emergency department with ACS symptoms a total of 842 times. Neither median prehospital delay time (experimental, 2.20 versus control, 2.25 hours) nor emergency medical system use (experimental, 63.6% versus control, 66.9%) was different between groups, although experimental patients were more likely than control to call the emergency medical system if the symptoms occurred within the first 6 months following the intervention (P=0.036). Experimental patients were significantly more likely to take aspirin after symptom onset than control patients (experimental, 22.3% versus control, 10.1%, P=0.02). The intervention did not result in an increase in emergency department use (experimental, 14.6% versus control, 17.5%). CONCLUSIONS: The education and counseling intervention did not lead to reduced prehospital delay or increased ambulance use. Reducing the time from onset of ACS symptoms to arrival at the hospital continues to be a significant public health challenge. CLINICAL TRIAL REGISTRATION: clinicaltrials.gov. Identifier NCT00734760.


Termination of resuscitation protocols.
Pubmed [4]
BACKGROUND: Despite the existence of national American Heart Association guidelines and 2 termination-of-resuscitation (TOR) rules for ceasing efforts in refractory out-of-hospital cardiac arrest, many emergency medical services agencies in the United States have adopted their own local protocols. Public policies and local perceptions may serve as barriers or facilitators to implementing national TOR guidelines at the local level. METHODS AND RESULTS: Three focus groups, lasting 90 to 120 minutes, were conducted at the National Association of Emergency Medical Services Physicians meeting in January 2008. Snowball sampling was used to recruit participants. Two reviewers analyzed the data in an iterative process to identify recurrent and unifying themes. We identified 3 distinct groups whose current policies or perceptions may impede efforts to adopt national TOR guidelines: payers who incentivize transport; legislators who create state mandates for transport and allow only narrow use of do-not-resuscitate orders; and communities where cultural norms are perceived to impede termination of resuscitation. Our participants suggested that national organizations, such as the American Heart Association and American College of Emergency Physicians, may serve as potential facilitators in addressing these barriers by taking the lead in asking payers to change reimbursement structures; encouraging legislators to revise laws to reflect the best available medical evidence; and educating the public that rapid transport to the hospital cannot substitute for optimal provision of prehospital care. CONCLUSIONS: We have identified 3 influential groups who will need to work with national organizations to overcome current policies or prevailing perceptions that may impede implementing national TOR guidelines.


Prehospital 12-Lead reduces door-to-balloon times

Head over to the Prehospital 12 Lead Blog

Pubmed [5]
BACKGROUND: American College of Cardiology/American Heart Association guidelines recommend greater than 75% of patients with an ST-elevation myocardial infarction receive primary percutaneous coronary interventions (PPCI) within 90 minutes. Despite these recommendations, this goal has been difficult to achieve. METHODS AND RESULTS: We conducted a prospective interventional study involving 349 patients undergoing PPCI at a single tertiary referral institution to determine the impact of prehospital 12-lead ECG triage and emergency department activation of the infarct team on door-to-balloon time (D2BT). The median D2BT of all patients (n=107) who underwent PPCI after field ECG and emergency department activation of the infarct team (MonashHEART Acute Myocardial Infarction [MonAMI] group) was 56 minutes (interquartile range, 36.5 to 70) compared with the median time of a contemporary group (n=122) undergoing PPCI during the same period but not receiving field triage (non-MonAMI group) of 98 minutes (73 to 126.45). The median D2BT time of 120 consecutive patients who underwent PPCI before initiation of the project (pre-MonAMI group) was 101.5 minutes (72.5 to 134; P less than 0.001). The proportion of patients who achieved a D2BT of less than or = 90 minutes increased from 39% in the pre-MonAMI group and 45% in the non-MonAMI group to 93% in the MonAMI group (P less than 0.001). CONCLUSIONS: The performance of prehospital 12-lead ECG triage and emergency department activation of the infarct team significantly improves D2BT and results in a greater proportion of patients achieving guideline recommendations.


Monitoring mean arterial blood pressure.
Umm.. See the first abstract. Luckily most modern monitors calculate this for us.

Pubmed [6]
OBJECTIVES: For some time, the inaccuracies of non-invasive blood pressure measurement in critically ill patients have been recognised. Measurement difficulties can occur even in optimal conditions, but in prehospital transportation vehicles, problems are exacerbated. Intra-arterial pressures must be used as the reference against which to compare the performance of non-invasive methods in the critically ill patient population. Intra-arterial manometer data observed from the patient monitor has frequently been used as the reference against which to assess the accuracy of noninvasive devices in the emergency setting. To test this method's validity, this study aimed to determine whether numerical monitor pressures can be considered interchangeable with independently sampled intra-arterial pressures. METHODS: Intensive Care Unit nurses were asked to document arterial systolic, diastolic and mean pressures numerically displayed on the patient monitor. Observed pressures were compared to reference intra-arterial pressures independently recorded to a computer following analogue to digital conversion. Differences between observed and recorded pressures were evaluated using the Association for the Advancement of Medical Instrumentation (AAMI) protocol. Additionally, two-level linear mixed effects analyses and Bland-Altman comparisons were undertaken. RESULTS: Systolic, diastolic and integrated mean pressures observed during 60 data collection sessions (n = 600) fulfilled AAMI protocol criteria. Integrated mean pressures were the most robust. For these pressures, mean error (reference minus observed) was 0.5 mm Hg (SD 1.4 mm Hg); 95% CI (two-level linear mixed effects analysis) 0.4-0.6 mm Hg; P less than 0.001. Bland-Altman plots demonstrated tight 95% limits of agreement (-2.3 to 3.2 mm Hg), and uniform agreement across the range of mean blood pressures. CONCLUSIONS: Integrated mean arterial pressures observed from a well maintained patient monitor can be considered interchangeable with independently sampled intra-arterial pressures and may be confidently used as the reference against which to test the accuracy of non-invasive blood pressure measuring methods in the prehospital or emergency setting.

94 yom CC: Chest Pain

Tom B | 11:22 AM | | 2 comments

Cross-posted to the Prehospital 12-Lead ECG blog.

Here is an interesting case submitted by Billy Eskridge.

EMS is called to an assisted living facility to evaluate a 94 year old female complaining of chest pain.

History of present illness:

Approximately 1 hour prior to EMS arrival, the patient had complained of a headache. A nurse gave the patient a Lortab. About 15 minutes later the patient started complaining of chest discomfort.

The nurse gave the patient two 0.4 mg NTG tablets over 20 minutes with no relief of the chest pain. The patient requested to be seen by a physician.

Paramedic evaluation:

Patient is slightly confused and lethargic but states that she feels "sick all over." The nurse states this is unusual for the patient.

Past medical history:

Complex medical history including hypertension, aortic stenosis, and mitral regurgitation

Vital signs:

Resp: 24
Pulse: 68
BP: 184/72
SpO2: 85 on RA


The cardiac monitor is attached.


A 12-lead ECG is captured.


Here are the computer measurements and interpretive statements.



Billy Eskridge asks the following questions:

Since this patient has an internal pacemaker and wide QRS complexes, is it possible to identify the ST/T changes of ischemia or acute injury?

I have also observed that not every beat is paced, and that there are come supraventricular beats which are also wide complex, showing a LBBB.

I know that there are certain tricks for diagnosing acute MI in LBBB, but I'm not familiar with them.

I am also aware that normal ST changes in wide complex rhythms can be used for diagnosis of MI if an old 12 lead is available to compare the current one to, but is this valid for both paced and supraventricular rhythms with a BBB?

If this rhythm was paces every beat without any apparent conduction abnormality can you scan it for AMI?


Discussion:

In the first place, even though the pacing spikes seem to "disappear" occasionally in the rhythm strip, it shows 100% pacing. I suspect that the pacing spikes are simply lining up perfectly with the lines on the graph paper, but regardless, we can rest assured that it's 100% paced because there is no change whatsoever in the R-R interval or QRS morphology.

In this case, the 12-lead ECG shows a fairly typical looking paced rhythm consistent with a pacing lead in the apex of the right ventricle. Namely, it shows LBBB morphology in lead V1 with a left axis deviation. It also shows negative concordance in the precordial leads, which is a common finding with paced rhythms.

You will note that the ST-segments and T-wave are deflected opposite the main deflection of the QRS complex (which is also the terminal deflection of the QRS complex). This is consistent with a "normal" paced rhythm and the "rule of appropriate T-wave (and ST-segment) discordance" with LBBB or paced rhythm.

Another important finding is that the larger the QRS complex, the more pronounced the secondary ST-T wave abnormality in the opposite direction. This is also true with strain patterns with left ventricular hypertrophy (LVH).

However, there are limits as to the expected amount of discordant ST-segment elevation in the presence of LBBB or paced rhythm.

According to Sgarbossa's Criteria, discordant ST-elevation (that's ST-elevation that is opposite the main deflection of the QRS complex -- in other words, ST-elevation in a lead with a negative QRS complex) > 5 mm is suggestive of AMI.

The problem is that QRS complexes with extremely deep QRS complexes will show more ST-elevation, and that's normal for LBBB and paced rhythm. For example, if you have a QRS complex in the right precordial leads with an S-wave that is 50 mm deep, you can have 5 mm of discordant ST-elevation and the ST-elevation is only 10% the depth of the QRS complex, which is fine.

Dr. Smith and colleagues from Hennepin County Medical Center propose a modified rule for discordant ST-elevation where you look for discordant ST-elevation that is 0.25 (or 1/4) the depth of the QRS complex.

Regardless, this 12-lead ECG shows a normal looking paced rhythm with appropriate T-wave discordance and ST-segments that are normal looking within the context of paced rhythms.

To learn more about Sgarbossa's Criteria and the "rule of appropriate T-wave discordance" see these previous posts:

Identifying AMI in the presence of LBBB - Sgarbossa's Critera - Part I

Identifying AMI in the presence of LBBB - Sgarbossa's Criteria - Part II

Merry Christmas 2009

Adam Thompson, EMT-P | 1:39 AM | | 0 comments

Merry Christmas from Paramedicine 101


Happy holidays to those of other faiths.

Be safe.



Thanks for stopping by,

Adam Thompson, EMT-P

Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.

Rogue Medic | 7:03 PM | , , | 5 comments





This study has received a lot of attention. I will interchangeably use the terms the IV (IntraVenous) group and the epinephrine group depending on the terminology I think is more relevant at the time. The distinction is not one that I believe is important. This is a study of IV medication in cardiac arrest. Epinephrine is the stated focus of the study.

There has never been any evidence to suggest that medication leads improved resuscitation outcomes. Unless your idea of an improved resuscitation outcome has nothing to do with quality of life.


Beneficial short-term effects of epinephrine have been shown in animal studies,3-5 but there is increasing concern for increased myocardial dysfunction6,7 and disturbed cerebral microcirculation after cardiac arrest.8[1]



Some people argue that the short-term effects are important. If we do not get a pulse back, we will not resuscitate anyone. This is true, but the problem is how much long-term damage do we inflict just to obtain that short-term improvement?

High-dose epinephrine is no longer recommended, even though it was better than standard-dose epinephrine at producing ROSC (Return Of Spontaneous Circulation). The current recommendation for epinephrine is based on this same misconception. More ROSC = better outcomes - except that the dogma is not supported by any evidence.


CONCLUSIONS--High-dose epinephrine (HDE) significantly improves the rate of return of spontaneous circulation and hospital admission in patients who are in prehospital cardiac arrest without increasing complications. However, the increase in hospital discharge rate is not statistically significant, and no significant trend could be determined for neurological outcome. No benefit of NE compared with HDE was identified. Further study is needed to determine the optimal role of epinephrine in prehospital cardiac arrest.[2]



That study was 17 years ago. That was far from the first study of epinephrine. There has been many studies of epinephrine in cardiac arrest since then.

We still do not have any research to show improved outcomes with any dose of epinephrine to treat cardiac arrest, but rather than admit that epinephrine should only be used in well controlled studies, we continue to make excuses. We are practicing alternative medicine, not real medicine.

Absence of evidence of benefit does not mean an absence of benefit, but when does it become enough evidence to insist that we stop using this ineffective and potentially harmful drug as the standard treatment?

Back to the current study.


Because there are no randomized controlled studies showing improved survival to hospital discharge with any drugs routinely administered during CPR, we concluded such a study was warranted.[1]



This study is possible because these researchers are outside of the US. In the US, the IRBs (Institutional Review Boards) seem to have concluded that it is unethical to deviate from the standard treatment, even if the standard treatment is harmful. Of course, we can never learn if the standard treatment is harmful, or even if it is beneficial, if we are prohibited from studying the treatment. However, the IRBs' definition of ethics seems to have been arrived at while consuming hallucinogens and reading Lewis Carroll.

Epinephrine in cardiac arrest is also firmly established outside of the US. Here is a part of their explanation of the study design.


In this prospective, randomized controlled trial of intravenous drug administration during out-of-hospital cardiac arrest, we compared outcomes for patients receiving standard ACLS with intravenous drug administration (control) and patients receiving ACLS without intravenous drug administration (intervention).[1]



ACLS is Advanced Cardiac Life Support - almost all of the treatments that would be given in the ED (Emergency Department). Not giving the drug is the intervention. Giving the drug is considered the non-intervention - the control against the effects of the treatment, which is the non-treatment.


Defibrillation was attempted in more patients in the intravenous group compared with the no intravenous group (47% vs 37%, respectively; OR, 1.16 [95% CI, 0.74-1.82]). More defibrillation shocks were delivered to those who received defibrillation in the intravenous group compared with the no intravenous group (median, 3 [range, 1-22] vs 2 [range, 1-26], respectively; P = .008). Both groups had adequate and similar CPR quality with few chest compression pauses (median hands-off ratio, 0.15 for the intravenous group and 0.14 for the no intravenous group) and the compression and ventilation rates were within the guideline recommendations (Table1).[1]



While there were no apparent differences in the quality of CPR, the more frequent defibrillations might be worth looking at. One of the important aspects of this study, as opposed to most prehospital research, is the recognition of a need to control for quality.

The explanation for the more frequent defibrillations that seems most likely is that the epinephrine produced a shockable rhythm more often than CPR alone produced a shockable rhythm. Since a shockable rhythm appears to be the next best thing to ROSC, this would not be a surprise. Many patients will change from a shockable rhythm to asystole when defibrillated. Defibrillation is a profound vagal stimulus and asystole is the ultimate vagal state. Even with similar initial rates of shockable rhythms, some of both groups would be expected to be shocked into asystole. The epinephrine, being a huge cardiac stimulus, would be expected to lead to a return of a shockable rhythm more often than just CPR. In other words, if the epinephrine is expected to produce ROSC more often, it should also produce a shockable rhythm more often. The authors came to a similar conclusion.


Without differences in the predefined primary outcome, patients in the intravenous group received more defibrillations, were resuscitated for a longer period, and more frequently had ROSC. With similar and adequate CPR quality, this is likely due to the pharmacological effects of the drugs used (epinephrine, atropine, and/or amiodarone). This finding is consistent with previous animal studies with epinephrine,6,7 and clinical studies evaluating the effects of amiodarone,23 atropine,24 and even high-dose epinephrine,25 all of which documented improved short-term effects without improving long-term outcomes.[1]



One major criticism of the methods is that they did not have a placebo to be given to keep the EMS crews blinded to the actual treatment. The authors do admit that this is a limitation. Of course, this placebo would probably not be called a placebo, since the epinephrine arm is the placebo arm, while the non-treatment arm is the active intervention arm, but that is really only an amusing problem of terminology and attitude. When the epinephrine group is the group with an IV line in place during resuscitation and the no epinephrine group is the one that does not have an IV until after return of pulses, there is not even an attempt at blinding. Did this lead to any detectable difference in the way patients were treated by EMS, other than other than the differences intended by the study design?


Our study has several limitations. First, ambulance personnel could not be blinded to the randomization. Closely related to this, only patients who were randomized to the no intravenous group could be monitored with regard to protocol compliance. If intravenous drugs were administered to a patient in the no intravenous group, violation of the study protocol could be
documented. If intravenous drugs were not administered to a patient in the intravenous group, several valid reasons could exist, such as rapid ROSC. We have no reason to believe that personnel refrained from establishing intravenous access under the pretense that the procedure was unsuccessful. The ambulance personnel involved were strongly committed to testing the hypothesis presented, but we cannot totally rule out possible bias toward procedures such as intravenous access and administration of drugs, which have been important in Norwegian culture for decades.[1]



This is a reason for creating a sham drug to use for the study. Without knowledge of the contents of the syringes being used, any bias of the treating medics should not affect the results. That is the purpose of blinding.


Analysis was performed on an intention-to-treat basis regardless of which treatment was actually given.[1]



In the No IV group, 10% received IV drugs. 9% of patients received epinephrine.

In the IV group, 82% received IV drugs. 79% of patients received epinephrine.

Why did some of the No IV patients receive epinephrine, or any drug? Clearly a protocol violation. I tripped and the IV landed in the patient, is not a valid explanation.

Why did 21% of the IV group not receive epinephrine? That is not clearly explained by the authors. Were these patients resuscitated prior to initiation of an IV and administration of epinephrine?

CPR and defibrillation are indicated before drugs. Since both CPR and defibrillation have research showing that they improve the long-term outcome from cardiac arrest, it is not unreasonable to expect that cases of ROSC with only CPR and defibrillation will be the reason for some patients not receiving epinephrine.

One of the perversions of a requirement that epinephrine be given in cardiac arrest is that the 1 mg bolus dose of epinephrine, repeated every 3 to 5 minutes, is never to be given to a patient with a pulse - Never. The reason is that epinephrine is so toxic to the heart, that it could be expected to produce cardiac arrest.

There are people criticizing this study because not all of the patients in the IV group received epinephrine. They see this as a bias. Contrariwise, I see their objection as just looking for any excuse to complain about research results they do not like, even though the study's results are consistent with all of the other research that has been done. The critics fail to consider that some patients will be resuscitated prior to the point in the algorithms where drug administration is indicated. Their apparent demand that patients resuscitated prior to epinephrine administration be given epinephrine, even though the patient is no longer in cardiac arrest, is silly.

This would also not be likely to do anything to improve outcomes in the epinephrine group. The patients resuscitated prior to epinephrine administration are likely to be the patients with the briefest periods of cardiac arrest and therefore maybe the patients with the best potential for good outcomes. Returning them to a cardiac arrest, by means of epinephrine, just to follow an algorithm, would not be a good thing and it would probably have a dramatic negative effect on the survival of the patients in the epinephrine group.

The standard dose of epinephrine for a patient with a pulse, but not in cardiac arrest, is 2 mcg/minute to 10 mcg/minute. The standard dose of epinephrine for a patient without a pulse, but in cardiac arrest, is 1,000 mcg fast push every 3 to 5 minutes. I do not know of any medical professional, or any medical organization, or any medical reference, that recommends giving a living human being the dose of epinephrine that we only give to dead patients, and repeating it every 3 to 5 minutes. I would not be surprised at murder charges if the patient were to die soon after receiving this treatment that is given indiscriminately to dead patients.

Unless we can predict which patients, if any, will benefit from epinephrine, we need to find a better way to prevent giving epinephrine to the patients who will be harmed by epinephrine. If we cannot do that, we need to admit that we do not have any basis for using epinephrine in cardiac arrest.

Until there is research to show any benefit from epinephrine in cardiac arrest, we should eliminate epinephrine from all cardiac arrest treatment algorithms that are not part of well controlled studies.


Footnotes:


^ 1 Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed - in process]

If you want to read the entire study, this link opens it in PDF.


^ 2 A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest.
Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J.
JAMA. 1992 Nov 18;268(19):2667-72.
PMID: 1433686 [PubMed - indexed for MEDLINE]


.

Video Laryngoscopy

Adam Thompson, EMT-P | 9:10 PM | , , , | 4 comments



With the advanced airway debate comes a need for solutions. Obviously increased training and QI/QA are at the top of the list. Another option is the Glidescope. This device is just one of a few video laryngoscopy devices that has shown phenomenal results. They are an expensive option, but probably cheaper than malpractice payouts. There is a ton of research out there regarding these devices. I have seen them used in the ER with great success, and I believe our helicopter has acquired one. Check out the video at the bottom.

Keep in mind that I am not the biggest advocate of prehospital intubation. Not until we improve our success rates and recognition of dislodged tubes. I believe laryngeal tubes and BVMs are the safer alternative as of yet. With that in mind, endotracheal intubation is the best way to secure an airway when performed adequately.

Pubmed [1]
BACKGROUND AND OBJECTIVE: We investigated whether the use of two different video laryngoscopes [direct-coupled interface (DCI) video laryngoscope and GlideScope] may improve laryngoscopic view and intubation success compared with the conventional direct Macintosh laryngoscope (direct laryngoscopy) in patients with a predicted difficult airway. METHODS: One hundred and twenty adult patients undergoing elective minor surgery requiring general anaesthesia and endotracheal intubation presenting with at least one predictor for a difficult airway were enrolled after Institutional Review Board approval and written informed consent was obtained. Repeated laryngoscopy was performed using direct laryngoscope, DCI laryngoscope and GlideScope in a randomized sequence before patients were intubated. RESULTS: Both video laryngoscopes showed significantly better laryngoscopic view (according to Cormack and Lehane classification as modified by Yentis and Lee = C&L) than direct laryngoscope. Laryngoscopic view C&L >or= III was measured in 30% of patients when using direct laryngoscopy, and in only 11% when using the DCI laryngoscope (P <>or= III: 1.6%) than both direct (P <>or= III) could be achieved significantly more often with the GlideScope (94.4%) than with the DCI laryngoscope (63.8%) Laryngoscopy time did not differ between instruments [median (range): direct laryngoscope, 13 (5-33) s; DCI laryngoscope, 14 (6-40) s; GlideScope, 13 (5-34) s]. In contrast, tracheal intubation needed significantly more time with both video laryngoscopes [DCI laryngoscope, 27 (17-94) s, and GlideScope, 33 (18-68) s, P less than 0.01] than with the direct laryngoscope [22.5 (12-49) s]. Intubation failed in four cases (10%) using the direct laryngoscope and in one case (2.5%) each using the DCI laryngoscope and the GlideScope. CONCLUSION: We conclude that the video laryngoscope and GlideScope in particular may be useful instruments in the management of the predicted difficult airway.



Teachable Moment

Adam Thompson, EMT-P | 8:38 AM | , , | 4 comments


At 0615 this morning I responded to a 33 year old female at a gas station, complaining of shortness of breath.


Upon arrival the patient was sitting down inside the business being assessed by FD. She was having a panic attack. Apparently she has had a long night of smoking crack, and drinking. She also had track marks up and down her arms. She stated that she ended up at the gas station after hitching a ride from a truck driver. She took something from the truck driver that was suppose to keep her awake.

I placed the patient in the back of the ambulance after a quick once over. After I made the judgement that she was not in any acute distress, I began my speech.
You have got to get your life together. A normal 33 year old woman does not get herself in these kinds of situations. This is the time, right now, that you need to get help. You are smoking crack, shooting up, hitching rides from truck drivers and taking random pills that they give you. You are dying. Your time is running out. I know you have probably heard this a million times, and it might not mean anything right now. I know this, but I am going to tell you anyways, because I do care, and I am sure someone out there cares too. You are only 33 years old, and you can live a whole different life, but only you can change that. Don't sit around waiting to be saved. Save yourself.

The truth is that this will probably not make any difference. After we offloaded the patient my partner asked me why I bothered wasting my time. I told her that you never know. The patient may be scared from the "medical emergency" and it may hit home. Everyone else that may have talked to her might have been a cop or someone else of authority. Sometimes it takes a medical professional. I know guys that have given up cheeseburgers because of something a doctor said. And cheeseburgers are good, really good. They might not be crack, but close to it.
If I get through to one addict in my career, I consider that a win. Give it a shot on your next call like this. Try to connect with the patient, and relate to their situation. You never know, you may save a life you never know you saved.

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