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Survivor gives us a lens into regional systems of care for acute ischemic stroke in North Dakota

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I just got back from the North Dakota Mission: Lifeline STEMI and Acute Stroke Conference in Bismark, ND. I had a great time and I learned a lot.

I often get asked to speak in various venues about acute STEMI and 12-lead ECG interpretation, but for this conference they wanted me to talk mostly about stroke. That turned out to be a good thing because it forced me to read the 2013 AHA / ASA Guildelines for the Early Management of Patients With Acute Ischemic Stroke to make sure I was asking intelligent questions during the panel discussion (which I moderated) and also giving accurate information for the class I taught about stroke recognition and treatment.

I also turned to a new source of information about acute ischemic stroke and that is the #FOAMed community on Twitter. If you're not familiar with FOAM or FOAMed it stands for "Free Open-Source Medical Education". I was surprised to learn that giving reteplase (Activase) or rtPA for acute ischemic stroke is somewhat controversial, at least in the emergency medicine blogosphere. That may explain why some of our emergency physicians locally are hesitent to give rtPA for acute ischemic stroke, especially for mild or rapidly improving strokes.

To help explain why rtPA is controversial for acute ischemic stroke I will refer you to a blog post entitled Schrödinger’s Fence at the Life in the Fast Lane blog.

This created some cognitive dissonance for me as I certainly didn't want to come across as a bomb thrower while moderating a panel discussion about acute ischemic stroke. In the end, it turned out that my concerns were completely unfounded because the panelists were happy to acknowledge that the therapy is controversial but well supported in the guidelines and give their reasons why they believed that rtPA is both indicated and underutilized for acute ischemic stroke. The panel discussion was video taped and I will update this blog post as soon as the video is available online.

What I really want to tell you about is a story of survival. But it's more than that. It's a story about love, and caring, and decision making, and even customer service.

As host of the Code STEMI Web Series as First Responders Network I have been priviledged to meet many STEMI and sudden cardiac arrest survivors, including the EMTs, paramedics, nurses, and physicians who  worked together as a team to save their lives. I have always imagined that the holy grail of survivor stories would involve therapeutic hypothermia, and actually being there at the bed side when the patient opens his or her eyes for the first time in the presence of their loved ones. 

At no time did I imagine how powerful a stroke survivor story could be. It simply never crossed my mind. So I was unprepared and deeply moved by a stroke survivor story that was presented on Wednesday.

The patient's name is Scott Onstine and his wife's name is Diane. Scott is a diabetic and the stroke affected the left temporal lobe of his brain. This area is involved in the rention of visual memories, processing sensory input, comprehending language, storing new memories, emotion, and deriving meaning. Scott sensed something was wrong so he contacted his wife by cell phone. This is critically important because as I learned this week, a huge number of stroke patients don't recognize their symptoms as stroke (perhaps because stroke does not cause pain) and it's not uncommon for stroke patients to "lie down" in attempt to "sleep off" the symptoms. This is a huge problem because time-to-treatment is extremely important for acute ischemic stroke and once stroke patients lie down, they usually don't get back up. Once they are found by a loved one it's usually either impossible to establish a timeline or it's too late to treat the stroke with rtPA.

Fortunately for Scott, his wife came home, thinking that perhaps his blood sugar was low. She tried to give him some orange juice but he threw it up. Then he knocked over the glass. She went up stairs and was shocked to see the bedroom completely trashed. Scott had been trying to use the phone, and because of his stroke symptoms, he couldn't figure out how to do it. Diane was getting scared, especially after she measured Scott's blood sugar and found out it was only 130. She contacted 9-1-1 with a certain amount of anxiety because she had called 9-1-1 once before thinking that Scott was having a stroke. On that occasion it turned out to be low blood sugar.

Diane got an awesome dispatcher. She rapidly determined that Scott was probably suffering a stroke due to his difficulty in forming speech. She actually had Diane perform a FAST (Face, Arms, Speech, Time) exam on Scott while waiting for the ambulance.

The test results revealed expressive aphasia. Diane spoke about how much this dispatcher meant to her, how she acted as a "life line" on the other end of the phone, keeping her calm and staying with her until help arrived. She spoke about a paramedic named Gus (who I also met); how kind, caring, and competent he seemed. She spoke about the firefighters who showed up on scene to assist, how professional they were, how they moved the furniture to make room for the gurney, and how they moved the furniture back.

She spoke about how Gus advised her that it would be a good idea to bypass the closest hospital and go straight to a Primary Stroke Center. She talked about how everyone kept her informed about what was going on, at this time when her life was spinning out of control. She talked about hearing the overhead page — a Stroke Alert in the Emergency Department — and how she knew it was for Scott, and how that reassured her that Scott was in the right place.

By this time Scott had taken a turn for the worse. He was barely responsive. A pastor showed up at the hospital and they prayed together at the beside. At the end of the prayer the pastor said "Amen" and they were both surprised to hear Scott say "Amen". She leaned over to him and said, "I love you!" He said, "I love you." Something deep in his soul knew that he was being prayed for, and that he loved his wife. He was receiving rtPA but they were simultaneously preparing him for an endovascular procedure due to the location and nature of the blockage in one of his cerebral arteries.

It turned out that the rtPA had worked and that blood flow had been restored to Scott's brain. He was rapidly improving. Before long, and had recovered almost all of his neurological functioning. He was discharged from the hospital and given a Holter monitor that revealed periodic atrial fibrillation. He now takes Coumadin to help prevent another stroke.

The Interventional and Stroke Neurologist Dr. Ziad Darkhabani made this simple observation. "Stroke is treatable and stroke is preventable."

This was truly one of the most powerful survivor stories I have ever heard, perhaps because it was seen through the eyes of the survivor's spouse. At the beginning of her talk, Diane made one of the most poignant statements of the entire conference. She said, "Strokes happen to a patient but they also happen to a family."

I have often thought about how any case study — good or bad — can provide a lens through which we can analyze a system of care from the patient's perspective. In this case we can see the entire stroke chain-of-survival. Scott didn't lie down. He called his wife. She realized it wasn't low blood sugar and contacted 9-1-1. The dispatcher recognized the signs of stroke and stayed on the line to encourage and reassure Diane. The first responders took the problem seriously, treated the patient with caring and competence, and provided excellent customer service by respecting the patient's property and moving the furniture back. Gus has the presence of mind to bypass the closest hospital for a Primary Stroke Center. The overhead page told Diane that the hospital was prepared for patients like Scott. They kept her informed. She was allowed at the bedside. She was treated with dignity, compassion, and respect.

Stories like this remind me why I got into health care. We need to celebrate our "wins" to keep us focused as health care professionals. System building isn't easy. In fact it can be very difficult. Couples like Scott and Diane make me realize that in the end it's all worth it. Although many believe the "jury is still out" on rtPA for acute ischemic stroke, it certainly appears to me that stroke patients do better within systems of care, and in hospitals with highly coordinated expertise at every level of care — prevention, diagnosis, and treatment — and dedicated units with nurses who specialize in neuro care.

We in EMS need to do a much better job in educating patients how to recognize the symptoms of acute stroke, and to encourage them to contact 9-1-1.

Special thanks to Mindy Cook from North Dakota Mission: Lifeline for inviting me to be a part of the North Dakota Mission: Lifeline STEMI and Acute Stroke Conference! Also to Peggy Jones, Coordinator of the Illinois Critical Access Hospital Network (ICAHN), who sat next to me at the conference and taught me a lot about the problem of patient delay. She is also a stroke survivor and an inspiring woman in her own right.

Also, to the EMTs, paramedics, nurses, and even a physician or two who stuck around for the 6:30 p.m. class on stroke and the 7:30 p.m. class on STEMI and 12-lead ECG basics, thank you! You guys totally rock! North Dakota is blessed with a truly dedicated group of health care providers.

Posted by on May 31, 2013 • Filed under: ems-topics, patient-management • Tagged: ,

The Trouble with Sinus Tachycardia

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Sometimes recognizing sinus tachycardia can give us fits.

What? Sinus tachycardia? One of the most basic rhythms?

The discussion that follows will highlight some of the difficulties sinus tach can present at high rates. The pitfalls of using the generalized term "SVT" will also be discussed. This discussion is not meant to imply that this issue is easy to navigate. It can get very difficult, and very dicey. The consequences of misinterpreting the rhythm and missing sinus tach can have very deleterious effects for our patients.

We are all good at recognizing sinus tachycardia at rates between 100-150, but when rates exceed 150 it seems to become problematic.

Is it difficult to recognize this?

No.

How about this one?

More difficult.

 

When sinus tachycardia occurs at high rates, our ability to correctly differentiate it from other types of SVT apparently decreases. P waves start to blend into the T waves. Instead of talking about discreet stand alone P waves, we talk about "notches" and "bumps". It is all too easy to look at a rate >150 and simply call it "SVT".

 

We know what sinus tach is: a sinus rhythm at rates faster than 100 (in adults), which is a normal physiological response to compensate for the increased needs of the body. I won’t spend time listing all of the possible causes, ranging from running around the block to septic shock.

AVNRT, a type of SVT that is responsive to Adenosine, is a re-entrant tachycardia that relies on a circuit through the AV node to sustain it. Block down the AV node, and the dysrhythmia terminates. Quite a bit different from sinus tach. Different mechanisms, different treatments.

Several case studies involving the above strips and ones like it have appeared on our FB page, and the FB pages of other EMS educational sites. What we have seen is that an alarming number of folks incorrectly identify sinus tachycardia as one of the other SVTs and want to treat with Adenosine or cardioversion.

Consider this rhythm strip that appeared on our page and another educational paramedic page:

The patient was a sick adult male, hypotensive. P waves are subtle, but they are there. Due to the rate, however,  a majority of providers (hundreds!) identified this as "SVT" and wanted to immediately cardiovert. 

Here is the followup ECG taken a couple of hours later. The patient was severely dehydrated and had received a few liters of fluid:

Now that the rate has slowed, sinus tach is clearly visible.

While we are discussing this, we should be clear about our terminology. Sinus tach is one of the Supraventricular Tachycardias. "SVT" is an umbrella term that represents a group of tachydysrythmias that originate above the ventricles. They will generally be narrow tachycardias, unless aberrant conduction is present. Some of the other types of SVT are AVNRT, AVRT, A-Flutter, A-Fib, junctional tachycardias and atrial tachycardia. Not only is sinus tach one of the SVTs, it is by far the most common SVT!

One of the issues that’s come to light is the fact that “SVT” is seemingly often taught as a “dysrhythmia” itself rather than what it really is: a group of dysrhythmias. I really don’t like the term “SVT” because it implies a diagnosis, when in fact it should motivate a provider to form a list of differentials and consider the H’s and T’s.

"Could this be sinus tach? A-Flutter? AVNRT?"

Treating "SVT" as a stand alone dysrhythmia leads folks to believe there is one “treatment” for SVT, when in fact the treatment is determined by which type of SVT the patient has.

What are we even taught about SVT?

Generally speaking these days, when students are taught SVT they are taught that a narrow tachycardia faster than 150 or 160 is "SVT". Simple as that.

How do we differentiate sinus tach from SVT?

That’s easy: rate!

If the rate is over 150 (some use 160), then it is “SVT and not sinus tach” and should be given adenosine or cardioversion! Quickly!

If you were taught that, raise your hand. Wow… that’s a lot of hands!

 

While we are on the subject, where did the rate limit of 150 or 160 come from?

I have NO IDEA. There does not seem to be any research I can find that even suggests that these numbers can be used to differentiate ST from other SVTs.

In fact, I could not find any research that demonstrates that absolute rate plays any part in differentiating ST from other SVTs.

All I could find is references to the guideline used to determine the theoretical maximum sinus tachycardia in healthy people: “220 – age”.

This “formula” is a guideline at best. It intends to illustrate that very young people can have ST at very high rates, and that as we age, it should be more difficult to achieve higher rates of sinus tach.  However, we deal with really sick patients, and theoretical guidelines are not good enough to help us with this issue.

What I know is what you all know. That medics are taught that at rates above 150, you can no longer see P waves, so you have to assume it is “SVT”.

“154= SVT”

“146= ST”

Easy as pie! Whether or not P waves are visible does not seem to factor into the equation.

 

Perhaps you don’t want to accept that these teachings do not seem to be based on anything concrete, but these are the facts. Sinus tach commonly exceeds rates of 150, and P waves are often discernable. More on this in a bit.

In any event, It is in this region of rates, between 150 and 200, where sinus tach is often mistakenly called “SVT”, and the risk of inappropriate treatment rises. Don’t believe it?

Before you can say “SINUS TACH”, I could show hundreds upon hundreds of comments left by medics stating that a rhythm “could not be sinus tach because the rate is over 150”.  And these comments were made by the medics who are motivated enough to visit educational sites and participate. 

The result of this is that too many medics are not correctly trained to deal with this issue. Sinus tach is unrecognized. The P waves are ignored, and the rhythm is labeled “SVT”, and the patient is in danger of suffering in more than one way:

For staters, they may receive an inappropriate treatment. A sick patient in sinus tach does not need to go through trials of adenosine, or even worse, cardioversion.  In addition to the discomfort, those treatments won’t work. Sinus tach is not a reentrant rhythm that relies on the AV node for its perpetuation, so adenosine or cardioversion won’t resolve the arrhythmia.

One of the most overlooked consequences of mistreating this rhythm is the fact that these patients are not getting the treatment they really need. These patients need lots of fluids. If medics are giving drugs and electricity, they certainly are not administering large boluses of NS.

It is easy to imagine how difficult the choice may seem. The sick patient in sinus tach will look shocky. He may have palpitations or chest pain, and may be altered. In other words, it will be very tempting to attribute the patient presentation to rate problem, even though the rate is compensating for their underlying medical issue.

Without a sound understanding of what sinus tachycardia really is, and what rate ranges are reasonable, it becomes much more difficult to make the right choice.

 

Probably right about now, some of you will want to blame ACLS for all of this. Consider the 2010 “Adult Tachycardia (with pulse)” algorithm [1]:

 

 

Box 1 states: “Heart rate typically greater than or equal to 150 if tachyarrhythmia”. 

What does that mean? What it seems to mean to a great many people is that a rate greater than 150 is "SVT".

If the patient appears unstable, we are performing synchronized cardioversion by box 4. There is no mention of sinus tach anywhere on this algorithm.

I’ll admit, I think that algorithm could be better. I think there should be a box that gets you out of that algorithm if sinus tach is recognized, similar to what appears on the ACLS Pediatric Tachycardia algorithm [2]:

 

 

Here, if the tachycardia is narrow, you are directed to one of two boxes which require you to assess for the presence of sinus tachycardia. I believe that a box like this in the adult algorithm would help clear up a lot of confusion.

In defense of the AHA, however, the simplified algorithm is based on the assumption that students have read the ACLS Provider Manual, on which the algorithm is based.

The following appears in the “Foundational Facts: Understanding Sinus Tachycardia” box on page 125:

           “Sinus tachycardia is caused by external influences on the heart, such as fever, anemia, hypotension, blood loss, or exercise. These are systemic conditions, not cardiac conditions. Sinus tachycardia is a regular rhythm, although the rate may be slowed by vagal maneuvers. Cardioversion is contraindicated.” [3]

Clearly, on page 125 of the ACLS Provider Manual, sinus tachycardia has been excluded from the adult tachycardia algorithm. It is a shame that fact is not reflected on the algorithm itself, because evidently a very large number of ACLS students do not read the manual and may incorrectly assume that rate is the determining factor.

 

I know some of you are thinking, “is this much to do about nothing? Is sinus tachycardia at rates above 150 as rare as an isolated posterior STEMI?"

We put this issue to the test. We brought in two well known electrophysiologists, Dr.’s John Mandrola and Mark Perrin, to shed light on this issue and share their perspectives with us. Readers of our blog will recognize them as past contributors and experts in their field.

I asked Dr. Mandrola about the utility of the “220-age” formula, and here is what he had to say:

           “The old formula 220- age equals the max heart rate represents only an estimate. It can vary by up to 10-15%. That's a lot. Normally a 30 year-old would have a max of 190. But with the variation, ST could be as high as 200. I see tons of patients for 'tachycardia', that's supposedly abnormal. Often its just ST. The short answer is that human heart rates vary quite a bit–at the high and low end.”

I then asked him what we really want to know: how common is ST at rates above 150:

          “The sinus node is highly innervated with both sympathetic and para-sympathetic neurons. Adrenaline can easily push the sinus rate above 150. Stress, anxiety, fever, dehydration, drugs, heat, and many other things can do this.  

            If a patient has upright p-waves and the diagnosis is ST and is unstable, it's not because of a primary electrical disturbance. ST is a sign not a primary arrhythmia. Patients with ST should be resuscitated, but not with shocks, with fluids, oxygen and rest perhaps and comfort perhaps.”

 

I asked Dr. Perrin for his thoughts about using a rate of 150 as a cut-off between sinus tach and other types of SVT and he had this to say:

            “Thinking that ST has an upper limit of 150-160 is kind of crazy. The septic, those in congestive cardiac failure, people with pulmonary emboli, hemorrhaging patients, etc, etc… all of these could hit heart rates of 190-200 or higher.

                 It is an easy diagnosis to make as well – because the P will always be present. Perhaps if the rate is > 200 it may disappear into the T wave a little. The only real differential is atrial tachycardia/flutter, and this is pretty unlikely to destabilize a patient.”

We discussed the issue medics are having in the field with inappropriate treatments of sinus tachycardia. I asked if he had any first hand experiences with it:

           "In fact, I have found, anecdotally, that paramedics are quick to shock patients. I have misgivings about this, especially for narrow-complex rhythms. We live in a city. ERs are close by. Why shock so quickly? There's some data that shocks harm the heart.”

My sincere thanks to Dr.’s Mandrola and Perrin for their contributions. As always, peer sourcing is great way to gain additional insight and expertise.

Hopefully this discussion has been educational for those who thought that 150 was any kind of limit for sinus tachycardia. The fact of the matter is that sinus tach at rates between 150- 200 not only exists, but is not uncommon. We need to be better at assessing for sinus tachycardia, because it is the most common SVT. We need to make sure we are doing right by our patients, giving them what they need and keeping them our of harm's way.

We also need to be better educators and providers.

Some will say, "we are teaching to the Registry", or "we are teaching to ACLS".  

They will say, "in the real world, they will know what to do".

From what I have seen, it doesn't work like that. Providers fall back on what they were taught, which often happens to be incorrect.

It begs the question, why are we teaching something we know is not correct? That can't be good for anyone.

For those who didn't know this information before, you know it now. Let's see if we can change the way we educate and provide care in this area.

It seems to be a deeply rooted problem, ingrained in decades of education. Time for a change. I don’t know if the issue has been raised before, but we are raising it now. 

As always, I look forward to your comments!

 

_

Footnotes:

[1],[3]-  Advanced Cardiovascular Life Support Provider Manual

                  2011, American Heart Association

[2]             Pediatric Advanced Life Support Provider Manual

                  2011, American Heart Association

 

Posted by on April 30, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

Episode #11 – Are we harming patients with oxygen?

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EMS 12-Lead podcast – Episode #11 – Are we harming patients with oxygen?

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In this episode of the EMS 12-Lead podcast we're joined by Kelly Arashin, ACNP, CCNS and Mike McEvoy, PhD, RN, CCRN, REMT-P at EMS Today 2013 in Washington D.C. We discuss the benefits and dangers of oxygen administration. 

Kelly is a dual boarded advanced practice nurse and Chair of the Hypothermia Steering Committee at Hilton Head Hospital in Hilton Head Island, SC.

Mike describes himself as a nurse, paramedic, firefighter, and medical college professor. He is also Chair of the Resuscitation Committee for University Teaching Hospital in Albany, NY.

Mike is the author of the article Can Oxygen Hurt? and taught an educational session at Physio-Control University entitled To Give Oxygen or Not: That is the Question. 

*** Update ***

Thanks to Brooks Walsh, M.D. for bringing this article to our attention:

Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality

Tom Bouthillet, Kelly Arashin, Mike McEvoy at EMS Today 2013

Special thanks to Physio-Control, JEMS, PennWell, and the ProMed Network

You can also watch the video version.

See also:

Follow Kelly Arashin on Twitter at @BarefootNurse24

Visit Kelly's blog

Follow Mike McEvoy on Twitter at @McEvoyMike

Visit Mike's website

Subscribe to the EMS 12-Lead podcast on iTunes

Posted by on March 27, 2013 • Filed under: ems-topics, patient-management • Tagged: , , , , , ,

Code STEMI – London Ambulance Service

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Ivan Rokos, M.D. has referred to primary PCI for acute STEMI as “the most complex, multi-disciplinary, and time-sensitive therapeutic intervention in the world of medicine.”

The emphasis on door-to-balloon times, and more recently, first medical contact or EMS-to-balloon times has transformed how acutely ill patients suffering heart attacks receive timely reperfusion in many communities, because as we’re so often told, “time is muscle.”

While some believe that the emphasis on door-to-balloon times has unintended consequences, in our opinion the real-life stories of the men and women who build these systems of care illustrate the very best of what modern medicine has to offer.

A single 9-1-1 call (9-9-9 in the UK) triggers an awe-inspiring series of highly coordinated events that clearly demonstrate that despite all of our arguments about health care and how it should be paid for, when a fellow human being is in danger, we will work together to save that person’s life.

We will exercise exceptional caring and competence, and then return that patient to their family. We give them another chance.

That’s powerful.

Many of us in EMS (and other areas of medicine) love survivor stories because it makes us feel good to know we’ve helped another human being. That’s why we got into medicine in the first place. But then something happened. We became jaded. We became cynical. We saw the worst in people.

The Code STEMI Web Series is a salute to the individual EMTs, paramedics, nurses, and physicians who had the courage and the insight to change the status quo and build something very meaningful that directly influences whether our friends, neighbors, or even our family members live or die.

Change can be difficult. It can be painful. It takes us out of our comfort zone and sometimes it rearranges the pecking order. Yet, we must change, whether it’s allowing EMTs to acquire and transmit a 12-lead ECG, activating the cardiac cath lab at 3:00 a.m. Sunday morning, or learning how to reduce “door-in to door-out” (DIDO) times at Critical Access Hospitals so that heart attack patients have the best possible chance of survival.

As Michael Hibbard, M.D. reminds us, it’s not the strong who survive. It’s those who are most able to adapt to change.

Our most recent episode of the Code STEMI web series looks at the London Ambulance Service. It is the busiest, and arguably one of the best EMS systems in the world. We interview front line EMTs, paramedics, nurses, and physicians as well as survivors. We hope you enjoy watching it as much as we enjoyed filming it so you can share our enthusiasm for witnessing a job well done.

Follow the #CodeSTEMI hashtag on Twitter!

Posted by on March 18, 2013 • Filed under: Dispatch & Communications, EMS Dispatch, ems-topics, patient-management, Uncategorized • Tagged: , ,

Code STEMI Web Series – London to premier at EMS Today in Washington, D.C.

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Seaon 2 of the Code STEMI Web Series is set to launch on March 7, 2013 at EMS Today in Washington, D.C.! This season starts out with our most exciting location ever — London, England as we feature the London Ambulance Service (LAS).

You can follow the series at First Responders Network or at CodeSTEMI.tv.

Special thanks to Physio-Control for sponsoring this web series!

Speaking of which, you can download the schedule for Physio-Control University at EMS Today by clicking here (PDF).

I'll be teaching an educational session called Hilton Head Island – Strengthening a Community's Chain-of-Survival. I'll explain how we achieved on of the highest cardiac arrest save rates in the nation (Utstein survival of 66% for 2012).

Hope to see you there! 

Posted by on February 24, 2013 • Filed under: ems-topics, patient-management, videos • Tagged: , , ,

47 year old male: Holiday Indigestion – Conclusion

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This is the conclusion to 47 year old male: Holiday Indigestion. Thanks go to a long time reader Nicholas Eisele for this holiday case! Editor's Note: sorry for the delay, it helps to press "publish"!

When we left off, our patient was in the back of the truck with a burning sensation radiating to his back. We had run a 12-Lead ECG and our partner was wondering which facility you wanted him to drive to.

To answer that question, we should look at the 12-lead!

Frightful Weather We're Having - 3rd 12-Lead

This 12-Lead shows a normal sinus rhythm at 70 bpm without ectopy or bundle branch block. A case could be made for incomplete right bundle branch block given a QRSd of ~110ms. Strikingly we have ST-depression in I, aVL, and V1-V5 with ST-elevation in lead III. Anytime you see flat or downsloping ST-depression in aVL you should look for elevation in the inferior leads (typically III). When present, it is almost certainly an inferior wall MI.

Frightful Weather We're Having - 3rd 12-Lead - III and aVL Closeup

Many readers commented that the ST-depression in V1-V5 could be either a sign of a posterior wall MI or a "anterior ischemia". It is important to remember that ST-depression from ischemia does not localize! This concept is so important, I'm going to list it again:

ST-depression from ischemia does not localize.

Traditional evaluation of ST-depression has taught that focal ischemia may cause localized ST-depression, however, this is not the case. Subendocardial ischemia causes diffuse ST-depression and will not be found in a localized pattern. Any time you have localized ST-depression you must consider it to be a reciprocal change first!

In our case, we have ST-elevation in lead III which clinches the diagnosis of an inferior wall myocardial infarction with possible posterior extension. A subsequent ECG revealed evolving ST-elevation in the inferior leads:

Frightful Weather We're Having - 4th 12-Lead

Remember, all patients who receive one 12-Lead should at least receive a second 12-Lead! If you were not comfortable activating a STEMI from the first clean tracing, serial 12-Leads provide improved diagnostic sensitivity. A single 12-Lead may only identify ~80% of STEMI patients.

The paramedics in this case recognized this fact, activated a STEMI alert, and transported the patient to their nearest PCI center. The in-hospital ECG showed continued evolution of the IWMI with the most impressive elevation and depression of the patient's clinical course:

Frightful Weather We're Having - In-Hospital 12-Lead

They achieved an impressive 83 minute first medical contact to balloon time with one stent placed in the RCA.

Frightful Weather We're Having - Cath Pictures

We hope you've enjoyed this case as much as we did, but more importantly this case presents some great teaching points:

  • Sometimes STEMI patients will have atypical symptoms.
  • A single ECG is not enough to detect all STEMI patients, serial 12-Lead ECG's should be acquired on all patients who receive one.
  • ST-depression from ischemia does not localize, localized ST-depression should be considered a reciprocal change until proven otherwise.
Posted by on February 19, 2013 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

47 year old male: Holiday Indigestion

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Thanks go to a long time reader Nicholas Eisele for this holiday case! As always, details have been changed to protect patient privacy.

It is a blustery Christmas morning when you and your partner are dispatched for a 47 year old male with chest pain. Firefighters are already on scene obtaining a history and vitals when you arrive.

You check in with the officer in charge, a paramedic, and he reports that the patient has been having a "burning sensation" in the middle of his chest, going to his back. As it is Christmas morning and the patient's family is opening presents, the officer also relays the patient, "is likely going to refuse." He also relays that they witheld ASA due to the patient's "indigestion."

One of the firefighters gives your partner the patient's vitals:

  • HR: 70 bpm, regular at the radials
  • BP: 144/96
  • RR: 18, unlabored, in no apparent distress
  • SpO2: 95%
  • ECG: "normal sinus, nothing out of the ordinary" (no 12-Lead was captured)

You perform a quick patient assessment prior to making any decisions:

  • Onset: 21:00 the prior evening
  • Provocation/Palliation: pain went away over night with sleep, came back after breakfast; nothing makes it better now
  • Quality: "burning"
  • Radiation: "straight thru to my back"
  • Severity: 7 of 10
  • Timing: constant burning

A focused history reveals no prior cardiac problems and that the patient takes no medications and has no allergies.

Given the patient's symptoms and possibility of a true cardiac problem you advise the patient that a trip to the hospital is worth it just to make sure he's not experiencing something serious.

After he sits down on your stretcher your partner begins placing electrodes for a 12-Lead as you gather four baby aspirin for the patient to chew.

Frightful Weather We're Having - Initial 12-Lead

You notice the artifact and hit print again, however, you decide you can run another one in the truck. After loading the patient your partner hands you the second 12-Lead, which is a bit cleaner than the first.

Frightful Weather We're Having - 2nd 12-Lead

Not completely satisfied, you run a 3rd 12-Lead in the back of the truck.

Frightful Weather We're Having - 3rd 12-Lead

Your partner asks which facility you'd like to go to.

  • What do these 12-Lead's show?
  • What are your next steps?
  • Is indigestion a contraindication to aspirin administration?
  • Are you glad this case does not involve a narrow complex tachycardia?
Posted by on January 24, 2013 • Filed under: ems-topics, patient-management • Tagged: , , , , ,

New Infographic: Left Anterior Fascicular Block (LAFB)

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Since infographics are all the rage nowadays I thought we'd put some together for ECG interpretation.

I'm starting with left anterior fascicular block… well, just because!

I hope you find these to be useful!

See also: Left anterior fascicular block

Posted by on January 23, 2013 • Filed under: ems-topics, patient-management • Tagged:

“What’s wrong with Mr. Wilson?”

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It is a sunny January afternoon at the ER when you are called to see a 57 year old male complaining of feeling "really sick".

You find your patient lying in the bed in room 3. He looks pale and short of breath. You introduce yourself and ask him why he has come in today.

He says:

"About two weeks ago, I started feeling short of breath, with a cough. I got much more tired than usual. I went to see my doctor, who said I had an upper respiratory infection and prescribed me some antibiotics. I rested at home for a few days, and started to feel a little better. Then, I began to go downhill again. Felt so awful today, barely have enough energy to walk, so I had my wife drive me to the ER."

He tells you that he has a history of hypertension and is a pack a day smoker, although he is trying to quit., Prior to getting sick, he has felt pretty well. In fact, he tells you that he started a work out regiment to lose some of the excess weight he is carrying.

Your patient tells you he hasn't been eating or drinking well lately, and he is hypotensive at 86/58.

As you are running through your list of differentials, the tech hands you this 12 lead ECG:

 

 

You take a look at the ECG, and a couple of thoughts come to mind. You have an idea of what might have happened.

You tell Mr. Wilson that you want to run a few tests…

So, what do you think is wrong with Mr. Wilson?

 

Posted by on January 19, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , ,

HyperK and Shades of Grey: Myths and Facts about Hyperkalemia Part II

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Today we continue our discussion about the myths and facts of hyperkalemia with Dr. Brooks Walsh, author of the Mill Hill Ave Command blog. We also feature contributions from Dr. Stephen Smith, of Dr. Smith's ECG Blog.

If you would like to refresh your memory on Part I visit here.                                         

Dr. Walsh and I spoke about why he thought hyperkalemia presented such a challenge for EMS providers:

"The recognition and treatment of hyperkalemia is one of those areas in medicine where, despite strong and clinically relevant results in the literature, the "usual practice" keeps kicking along. This is like a lot of areas in medicine, true."

With that said, let us continue with Myths and Facts about Hyperkalemia Part II:

 

Myth: The ECG shows a predictable sequence of changes as the potassium level increases

Experiments done on (presumably) healthy animals demonstrated a progression in ECG derangements as potassium levels were experimentally raised. A number of textbooks and review articles repeat this result, even though numerous human clinical studies have failed to replicate a linear relationship between the potassium level and specific ECG findings.

For example, one review article, much referenced in the EM literature, presents a table describing the correlations between potassium levels and expected ECG findings.

 

But the literature is full of case report that argue against such tidy correlations: here's a case of a woman with a potassium of almost 8, and complete AV block  but no QRS widening or T-wave tenting; here is a similar case with a K of 7.5; we even see that a patient can develop an AV block with a K level of just 5.5! On the other hand, here's a case of complete AV block with a narrow QRS, but a potassium of just 6.4.

We asked Dr. Stephen Smith about his experiences with this issue. He agreed and said he has seen patients go into VF after having only peaked T waves. You can see examples of this here.

So it seems better to avoid thinking that you can determine a specific potassium range on the ECG, but rather that it can suggest a generally elevated level. Any of the "expected ECG abnormalities" can occur at any level of potassium.

 

 

Myth: Calcium is a dangerous medication

Make no mistake – IV calcium can be a potent drug, but with potential benefits. And you should always refer to your local guidelines/protocols for the last word on when you can & should give it.  

But that being said, there is some concern voiced by clinicians about administering "one mustard box." Let's talk about 2 big concerns that people seem to have with giving calcium: skin necrosis and digoxin toxicity.

So, how worried should you be about skin necrosis? EMS usually carries calcium chloride, which has some potential to cause problems if it extravasates (calcium gluconate has a lower risk, and can be given subcutaneously for some problems). As a result, many people have a lot of concern about administering the medication, fearing the risks if the IV leaks or fails. 

Well, yes, you must assure yourself that you have a patent, free-lowing line in a big vein! But on the other hand, you have already been taking risks with injecting dextrose 50% and sodium bicarbonate, as both are known to cause skin necrosis. 

For example:

 

 Ann Emerg Med. 2006;48:236

This patient came into the ED with hyperkalemia, and was treated with IV insulin and dextrose (no calcium). 

Or how about this hand?

 

Ann. Surg. – November 1975

That's a neonate who was getting a D10% drip in his hand.

There are a small number of case reports of bad calcium extravasations, but that rare risk must be balanced against the immediate, and unpredictable, risk of life-threatening arrhythmias.

Some EMS-toxicologists may also point to the historical concern with digoxin toxicity, that calcium infusions could provoke a "stone heart," or cardiac tetany. A recent pig study had cast a lot of doubt on that thinking. And then a retrospective study was published in 2012 by Levine et al., which looked at patients with digoxin toxicity, some of whom were also treated with calcium. They found no effect on mortality – no "stone heart ' – and another myth was dispelled.

 

 

So you should feel comfortable giving calcium when you think you're dealing with hyperkalemia. But don't just take my word for it – listen to some medical experts!  

For example, from a nephrology paper:  

 "When uncertain of the importance of a raised potassium level, it is prudent to go ahead and administer calcium gluconate, as the downside risk is minimal."    Aslam 2002

Again, ECG master Stephen Smith:

"[G]iven the fact that calcium therapy is benign… when I suspect hyperkalemia I just given calcium immediately, even before I get the potassium back. … There are so many ways the ECG can manifest with severe hyperkalemia — life-threatening hyperkalemia. Again, the treatment is benign, and cheap! So how many life-threatening diseases can you treat benignly and cheaply?"

You can hear Dr. Smith expand on this by listening to him on  EMCRIT podcast 42.

 

 

Practical point: How to give albuterol for hyperkalemia

Albuterol may in fact have a role in the prehospital treatment of hyperkalemia. It works by shifting potassium from the serum into the cells.

Consider this case study abstract:

"Growing evidence suggests that there may be a role for albuterol in the treatment of patients with severe hyperkalemia…β2 agonist administration was found to be safe and was associated with a significant decrease in serum potassium levels. Therefore, β2 agonist therapy should be considered as an adjunctive treatment for patients with severe hyperkalemia."

Or this:

"In the doses used, nebulized albuterol therapy resulted in a prompt and significant decrease in the plasma potassium concentrations in patients on hemodialysis, and caused no adverse cardiovascular effects (Allon).

You can use an albuterol in a nebulizer, or can use levalbuterol if that's what you have (Pancu). And it doesn't have to be a neb – it can also be an MDI with a spacer (Mandelberg).

But how much to we give? Of the medics who are savvy enough to want to use Albuterol to treat hyperkalemia, few of them know the effective dose needed to treat.

You can give 5mg (McClure), 10, or even 20mg (Allon), if you are using a nebulizer. The dose of 10-20 mg seems to be the dose most often used. 

Perhaps you realize that the "standard dose" we use to treat bronchoconstriction is 2.5mg/3ml. It is problematic to consider loading at least 4 doses into a small volume nebulizer. That's not really going to work. 

Albuterol does come prepared as 2.5 mg/0.5ml. Now we are talking about 2 ml's, which is much easier to manage and a better choice for treating hyperkalemia.

Is it worth stocking multiple doses of Albuterol? Perhaps. It is not going to be the first line treatment for hyperkalemia, so the decision will vary by system. Needless to say, if you are going to treat with Albuterol, make sure you have an effective way to do it.

 

We hope you have enjoyed this short series on the Myths and Facts about Hyperkalemia. 

My thanks again to Dr. Brooks Walsh, as well as Dr. Stephen Smith for their valued contributions.

As usual, all comments and opinions are encouraged!

Posted by on January 14, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,