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63 Year Old Female, CC: Neck and Arm Pain

14 comments

 

Good morning. It's 7:45 am on a sunny winter Monday, and you are just finishing up your holiday shopping list– it is getting down to the wire after all!

The tones go off, and you are dispatched to the residence of a 63 year old female, "sick". 

You arrive to a well kept two story suburban home. You are met by a well looking gentleman who directs you and your partner into the living room, where you find his wife sitting on the sofa looking slightly uncomfortable.

"How can we help you today?"

"Well, i'm having strange pain in my neck and both arms… feels like pins and needles too.."

"Any chest discomfort?"

"A little bit… a little tightness across the front of my chest."

As you continue with the history, she denies any difficulty breathing, lightheadedness, or nausea. She tells you the discomfort woke her from her sleep at about 6 am… she thought it would go away, but it didn't so her husband called 911. Nothing seems to change the discomfort, and she tells you that she is generally in good health–this has never happened before.

Her past history is significant only for hypertension. She was a two pack a day smoker, but she quit 5 years ago.

Your partner acquired the following set of vitals:

  • Pulse: 54, irregular
  • BP: 122/68
  • RR: 18 regular, lungs clear
  • SpO2: 99% RA
  • Skin: slightly pale, warm and dry

 

You acquire the following 12 lead ECG:

case12:16

 

Your patient tells you the discomfort is "not that bad", and asks if you could give her something for it now–she doesn't want to go to the hospital.

What do you tell her?

You are 15 minutes from the local hospital, and about 50 minutes from the nearest PCI center.

 

  • What is your field diagnosis (yes, I did use that word)?
  • What are the significant findings on the 12 lead ECG?
  • What is your treatment plan?
  • To which facility will you transport your patient and why?
  • Are there any other treatment considerations for this patient?

 

Thanks for reading, and looking forward to your comments!

Posted by on December 16, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , ,

Why do we send so many people to a cardiac arrest?

30 comments

pitcrew

I did a fair amount of traveling and teaching in 2013 and I've been struck by the number of people who have been gobsmacked by the number of rescuers my fire department sends to a sudden cardiac arrest (1 ambulance, 2 engines, and a battalion chief).

I think there are several reasons for this. In the first place, most jurisdictions don't have the resources, or at least say they don't have the resources, to do what we we do. But I think the real issue is that people don't understand the benefit of sending 9 to 11 people to a sudden cardiac arrest. In fact, some have argued that sending that many people only encourages therapies (like drugs and tracheal intubation) that have not been proven to positively effect neurologically intact survival. 

I disagree. The two issues are not related.

Aside from the fact that we identified this additional staffing on the first alarm as a best practice after speaking with some of the best EMS systems in the country (those few who can prove it), let's look at the big picture.

First, we need to consider that sudden cardiac arrest, particularly witnessed VF arrest, is a survivable event — when a process is in place to save that life. Although I don't take credit for the maxim, I have said many times that "every system is perfectly designed to achieve the results that it gets" and I certainly believe that. If the planets need to be in perfect alignment for a patient to survive in your system then it is not geared to save lives. Rather, it is geared to take patients to the hospital and generate revenue.

You might deliver excellent customer service, and you might have talented EMTs and paramedics, but no individual can save lives in a vacuum, or at least, very rarely can they manage to do that. Human performance is inexorably intertwined with system performance. Almost every young, highly intelligent, and motivated paramedic who becomes disillusioned with his or her EMS system is told, "just do the best you can in the back of your ambulance and make a difference with each and every patient you come into contact with." You can try to do that, it's true. I'll even conceded that you can find some value or solice in doing that.

But you cannot reach your potential as a medical professional within a poorly performing system.

Poorly performing systems are almost never the fault of the guys and gals on the front lines. That's true in factories, it's true in the military, it's true in hospitals, and it's certainly true in EMS systems. You can achieve compliance with a whip but you cannot achieve quality. Once we accept that it's all about the process, we can go about the task of designing processes to save lives.

The principles of the 2010 AHA ECC Guidelines are quite simple.

  • Minimally interrupted chest compressions
  • Controlled ventilations
  • Early defibrillation and shocking in a 2-minute cycle
  • Managing the peri-shock pause
  • Allowing capnography to identify ROSC 
  • Early identification of STEMI and transport to a PCI center
  • Ensuring that eligible patients receive targeted temperature management

As they say in the Resuscitation Academy in Seattle, "it isn't complicated but it's not easy." The reason it's not easy is that while no individual piece is particularly complicated, making it all happen in a highly coordinated way involves a lot of different individuals who must work together as a team, and do so over and over again, with different team configurations.

The issue is variability — the enemy of system performance.

So why send so many people to a sudden cardiac arrest? Here are the benefits.

1.) Experience

You might have a brand new paramedic on the first arriving ambulance. But when you send multiple assets to the call you're bound to get an experienced paramedic. I can already hear the objections from some of you about "skill dilution" (which I think pales in comparison to the modern problem of "never having the skill in the first place"). But, the reality is, leaving newer paramedics alone to experience clinical misadventure teaches them nothing, except perhaps "what happens in the back of the ambulance stays in the back of the ambulance". Which brings me to the next point.

2.) Modeling

A very important, but initially unanticipated, side benefit to sending multiple crews to a cardiac arrest call is that each time we assemble our Pit Crew CPR process is an opportunity to model the correct behaviors for our personnel. We are able to reinforce our checklist-driven methodology that ensures that the appropriate leadership and communication take place, that we do not move patients in cardiac arrest prematurely, that we meet important benchmarks, and that we do so in a calm and organized fashion.

checklist

3.) Logistics

There is absolutely no reason that the first arriving crew to a sudden cardiac arrest should have to worry about locating the patient, carrying the cardiac monitor, airway bag, suction unit, drug box, a backboard, 2 liters of iced saline, and a gurney onto the scene of a cardiac arrest, which could be on the 5th floor of a hotel. When you send enough appropriately trained people to a sudden cardiac arrest you can have people holding the elevator, interact with the family, run back to the ambulance, switch out the rescuer on chest compressions, take a 30,0000 foot view and act as a "code commander", be a scribe, or just put another set of eyes on the process.

4.) Leadership

Taking command of a structure fire is considered so important that failure to do so is considered negligence in the fire service. The reason is simple. When we act as individuals (freelance) we get into trouble. There may be confusion about whether or not we are "offensive" or "defensive", vital information may not be shared, dangerous ventilation practices can threaten interior teams, or there can be a catastrophic loss of situation awareness that leads to firefighter death or injury. Have you ever been on a call with three paramedics and seen them work separately as opposed to as a team? Someone must be in charge. That doesn't mean someone reverts to Theory X and becomes unapproachable or dictatorial. It means that someone coordinates the team's activities. To do this effectively on a system-wide basis requires specific training in crew resource management which is outside the scope of this blog post.

5.) Supervision

When you send a supervisor to each and every resuscitation attempt it helps to ensure consistency from crew to crew and shift to shift. It also helps cut through any issues or problems you might have on scene. Our battalion chiefs often act as the family liaison, interact with law enforcement, nurses, or physicians on scene, make sure that policies are followed, and sometimes, even provide expert clinical care if the need arises. They are there to support the personnel who are engaged in the resuscitation, and they are there to monitor performance to identify opportunities for improvement.

In the beginning, there were plenty of paramedics who bristled at the idea of a battalion chief showing up for resuscitation attempts, and some of them thought a second engine was a ludicrous waste of time and money. No one feels that way anymore. In part, that's because we measure our outcomes and the increase in neurologically intact survival, particularly in calendar year 2012, was undeniable. When you have 9 additional survivors who walked out of the hospital (or were at least rolled out in a wheelchair) in a department the size of mine, it means that the majority of the department participated in at least one save.

That's pretty good for morale.

We have spent the last 20 or 30 years sending half the fleet to a "pot on the stove". Now, everyone understands that a sudden cardiac arrest is just as important (actually far more important) than the average "smoke in a structure". That's a change in culture. There have been other changes, too. Like the idea that we provide supportive and non-punitive feedback to the line. It turns out that when you believe in people, provide the appropriate education and training, explain the "why", give them the right tools to do the job, and support them, they rise to the occasion and do amazing things. They help build a process that saves lives and they take ownership of it. They should, because we can't do it without them. It's a human being that performs chest compressions, starts IVs, charges a defibrillator, and makes critical decisions.

A lot of people say "response times don't matter" or "it's such a small percentage of our call volume". Well, to say the least statements like that require qualification. I find it to be far more palatable from an EMS system that knows its numbers and has optimized its system performance. Otherwise, we're essentially writing off our most critical patients. I got into this business to save lives, and I'll bet you did, too. Then, somewhere along the way, we became cynical and jaded.

Saving lives makes you believe again. It feels good, too.

Posted by on December 7, 2013 • Filed under: ems-topics, patient-management • Tagged: , , ,

The Weekend Roundup: ECG Highlights from Around the Web…

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weekend-roundup                                                                                                                          *image credit

In case you missed it this week:

 

We had a great case discussion regarding an equivocally challenging ECG.. Was it pericarditis in the end?

 

Dr. Smith had a great case about Wellens' and the implications for treatment.

 

Amal Mattu's ECG video of the week tackles the Modified (yes, a nod to Dr. Smith!) Sgarbossa Criteria.

 

How good are your arrhythmia recognitions skills? GE Healthcare has this Arrhythmia Quiz, 24 questions, with a good review of the essential rules of interpretation!

 

Dr. Venkatesan wonders… "Is it a crime to treat ACS withoug knowing coronary anatomy?"

 

K. Wang presents a new ECG Video covering electrolyte disturbances.

 

Theblunddissection has a quick trauma ECG case involving a 42 year old male c/o chest pain following an MVA.

 

Important Cardiac Arrest news from Wake County showing evidence that we should work cardiac arrests until ROSC or ETCO2 < 11.

 

In this video, Dr. Sheldon Cheskes discusses his study regarding the Peri-shock Pause.

 

Don't forget to check out the latest from the Code STEMI Web Series!

 

Have a great weekend!

 

 

 

Posted by on November 8, 2013 • Filed under: ems-health-safety, ems-topics, news, patient-management, videos • Tagged: , , , , , ,

37 Year Old Male–CC: Chest Pain, Part II

3 comments

This is part II to "37 year old male–CC: Chest Pain". You may wish to review the case.

So, while many of our cases are straightforward, this one is not. 

But hey, our patients don't read the textbooks!

First, let's review the chief complaint: 

Our 37 year old male had "chest tightness", but complained of lethargy and "chills" for at least a couple of days. While we must take the complaint of chest pain seriously, many of you pointed out that the history did not seem like typical ACS. We can't blow off chest tightness, but the history is no slam dunk. 

Here again is the 12 lead ECG:

casestudy9:13-1

There is sinus rhythm at a rate of about 83 bpm. Axis is normal. QRS is slightly widened. PRI is normal, and we can debate whether or not there is slight PR segment depression. There is some artifact present. Using the TP segment, there is slight (<1mm) STE in leads II, III, aVF, V5 and V6. If you use the PR segment, which may have some slight depression, you will see a bit more ST elevation. All ST segments are upsloping. Regarding V2-V4, is there any ST elevation? Some will say yes, but there is some wandering of the baseline, and I am not convinced. If there is any, it is a small amount. All ST segments seem to be concave up. There is no reciprocal ST depression. We do not have the computer interpretation/measurements for this ECG. 

What do we make of this ECG? Again, as in the history, no slam dunk. I think we can realistically consider three possiblities:

  • ACS
  • Pericarditis
  • Early repol

ACS: Was it reasonable for the crew to run this as ACS? I think so. Even if the story sounds a little odd, we can't rule out ACS based on anything here. Does the ECG show STEMI? The constellation of changes we have is not really consistent with the ST elevation of STEMI. Some may point out the inferior ST elevations, but where is the ST depression in aVL? We don't have it, and if it were inferior STEMI we should see it. In fact, there does not seem to be any reciprocal depressions anywhere.

In his most recent post, Dr. Smith writes: "Does inferolateral STEMI also have reciprocal depression in aVL? In my experience, yes. I have yet to see an inferolateral STEMI without some reciprocal depression in aVL, in spite of the lateral ST elevation in V5 and V6". 

We can treat for ACS, but I don't think anyone is activating the cath lab based on this ECG.

Pericarditis: The favorite choice in the comments section was pericarditis. The history, especially feeling "sick" with "chills" for a few days opened up the possibility of infection. On the ECG, we have some widespread ST elevations, although not a large amount. There seems to be some slight PR depression, which is why I used the TP segment to measure the STE. The axis is towards lead II but slightly away from aVL, so I think the axis is somewhere between 70-80 degrees. This could be consistent with pericarditis, which is usually towards 60 degrees. 

Early Repol: Could this be early repol? With slight concave up ST elevation, it could also be early repol and his normal baseline ECG.

Playing the odds, we can recall that pericarditis is in fact a relatively rare diagnosis.

In his most recent post, Dr. Smith writes that "baseline inferior ST elevation (early repol of the inferior leads) is more common than pericarditis, and if a patient complains of chest pain, and happens to have baseline inferior early repol, they are likely to get a diagnosis of pericarditis if they rule out for ACS".

 

How do we manage our patient? I don't think we can tell from this one ECG what the issue is. The ECG is non-diagnostic. As I said earlier, I think it is reasonable to treat for ACS. While this case may not scream ACS, we can't rule it out either. It doesn't appear to be STEMI, so I don't think we need to activate the cath lab.

Supportive care is in order, but what I really think would be helpful are serial ECGs. We may see evolutionary changes of ACS or of pericarditis, or we may see no dynamic changes at all. But it would probably give us more insight into his condition. 

In the ED, echo and troponins would likely give us the diagnosis. 

So how did the crew handle our patient? They opted to activate the cath lab and treat with ASA and NTG. Upon arrival at the cath lab, the cardiology team is split as to what to do before finally deciding on angiogram to rule out any blockages. The cath was clean. 

The final diagnosis was "reaction to medication". Apparently he had not been compliant with how to take his regimen of pain meds.

This case was not straightforward, but sometimes these types of cases can be the most interesting. They inspire a lot of great comments and discussions as well. Thanks to all who participated! 

 

 

 

Posted by on November 4, 2013 • Filed under: ems-health-safety, patient-management, Training, training-development

37 Year Old Male- CC: Chest Pain

29 comments

This excellent case comes to us from Paramedic Jack Buckle. Thanks Jack!

You and your partner are in the middle of a busy shift, when you are dispatched to 37 year old male complaining of chest pain.

It's almost 2pm, and a balmy 78 degrees.

You arrive to a well kept house and find your patient sitting in his kitchen. He looks pale, but you don't notice any obvious distress.

"How can we help you today?"

"I just haven't felt well for a couple of days. No energy. Chills.  And I've been nauseous."

"What made you call 911 today?"

"Well, to be honest, I started having some chest tightness today and I got really scared."

His discomfort, 6/10, is poorly localized and non-radiating. He describes it as "intermittent". It started when he was at rest, and began about 2 hours prior to calling 911.

After talking with your patient, you understand that he suffers from depression stemming from a rugby accident that left him with a severely painful back condition.

In fact, he has previously undergone L5-S1 fusion surgery. He takes several pain meds for this chronic condition.

Although he states that during a recent hospital stay (related to back pain) he had to be on the cardiac monitor (he doesn't know why), he denies any history of cardiac problems, and no allergies.

Vitals:

  • Pulse: 78 regular
  • BP: 141/90
  • RR: 20, unlabored
  • SpO2: 99% on high flow O2
  • Skin: pale, cool and dry

You acquire the following 12 lead ECG: 

 

You are 14 minutes from the community hospital, and 22 minutes from the nearest PCI center.

 

YOU MAKE THE CALL:

What do you think is going on with this guy?

Where should you take him?

How should you treat him?

 

 

Posted by on September 9, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , ,

“Treat the patient not the monitor?”- Redux

10 comments

 

"For heaven's sake man, treat the patient not the monitor!" 

Ahh, the angry cries appear every time we post a difficult case with a challenging ECG or treatment decision..

The attitude seems intractable, despite our best efforts.

Over a year ago, I wrote "Treat the Patient not the Monitor?", and not much has changed since!

So, I got to thinking. Where did this come from anyway? What were the intentions of the originators of "treat the patient not the monitor"?

In search of answers, I visited treatthepatientnotthemonitor.com, but surprisingly found nothing.

I am left only with my theories and opinions.

Back in the day, decades ago, I'm sure all of this wasn't an issue:

                                                                                                                  *Bonus points if you know who this is!

*image credit

 

Pulse-ox? Portable cardiac monitor? I don't think so!

However, as the advent of portable medical devices made its way to EMS, educators and skeptics alike told cautionary tales about not treating "the monitor"– just look at your patient!

There are the classic examples we are all familiar with :

You put the pulse-ox on the patient with good color and no signs of respiratory distress and it reads 88%. 

HE NEEDS O2 STAT!  Well, of course not, because we treat patients not monitors!

Because measuring blood glucose is considered a "vital sign", you check it on an A/O patient (come on, you know some of you do it) and it reads 62.

HE NEEDS DEXTROSE STAT!  Well, again, not so fast, because we are treating patients not monitors!

It is a good lesson, right? We do not treat numbers on a machine, we treat living breathing patients, and sometimes we just don't know what to do with the numbers.

By the way, cardiologists are having somewhat of a similar issue with high sensitive troponins. Because they are so sensitive, more patients without acute ischemic heart disease are showing positive readings, and now it is not clear what to do with all of them.

In Treat the Patient Not the Monitor -Part I, Rogue Medic writes that citing these words is "dangerous in the wrong setting".  I couldn't agree more.

What exactly is the wrong setting? What is the right setting for that matter?

For starters, it comes back to our patient assessments. Can we assess a patient without the help of technology? Of course we can. 

Will that assessment be as thorough and accurate as it could be? Well, maybe not!

Our technology is a key part of our assessment. If used in the correct setting, it adds information that we might not have been able to obtain otherwise.

The key word, though is "Context".

We should have a reason to use whatever technology we are using. In the setting of an AMS patient, getting a blood glucose reading makes sense to me. It is the proper context.  If a patient is short of breath, pulse pulse-oximetry, or even better, capnography makes sense to me. If a cardiac etiology is the suspected cause of a patient's presentation, the monitor makes sense.

What does not make sense to me is the blind usage of this technology on every patient. I know it is done. I know people can make good arguments for that, but it doesn't work for me.

Here's why. Without the proper context, I feel like i might not know what to do with the results.

As I mentioned earlier, many medics routinely obtain blood glucose readings on every patient as a "vital sign".

My dilemma is this: Do I have a clinical reason to obtain this information? Will it alter the way I treat my patient?

Does he have a CVA or hypoglycemia? Of course, I'll check the BGL. But check it on everyone?

If i do this, what happens when I get a reading of 62 on an alert and oriented patient?

I have two choices:

Option 1: I treat the number and give my patient glucose. Well, I'm not going to do that, because my patient is not altered and doesn't need it.

So I go for Option 2: I simply ignore the number. Write is off as an "erroneous". 

The problem is, If I am not going to use the reading I obtained, why am I getting it in the first place?

I don't use pulse-oximetry on everyone, and I don't routinely obtain a 12 lead on every patient encounter either for the same reasons. 

I realize that right now, many of you are thinking, "see, even HE treats the patient and not the monitor!"

This is where i differ.

It all comes back to context. Clinical judgment means using all available information to assess the patient and find out what is going on. Of course, that does not mean blindly following the monitor, but it certainly does not mean ignoring it.

The reason "Treat the patient not the monitor" does not apply to the cardiac monitor is that used properly, it can give us information that we could not otherwise obtain. You can not look at a patient and determine whether or not he is having a STEMI. 

Do we still examine our patients? Hands on, getting a feel for the pulse, their skin condition? Of course we do. But there is so much more to assess.

The fact is, there is no other surrogate for the monitor. We can not "look at our patients" and have an idea of what the monitor will reveal. That is quite different from blood glucose, NIBP, pulse pulse-oximetry, etc where there will be signs and symptoms of what those "monitors" will show.

The cardiac monitor? You just won't know until you apply it.

You might feel a slow regular pulse, but you don't know if it is Sinus Brady, Mobitz 1, or complete heart block.

That rapid pulse you palpated? Is it VT, AVNRT or A-Flutter? 

Is there a STEMI, sending them straight to the cath lab?

Is that Brugada in your syncope patient?

Maybe it's WPW or ARVD!

To be blunt, in many cases you simply can't diagnose (yes we do that) your cardiac patient correctly without the monitor:

 

There are limitations to the cardiac monitor. They need to be troubleshooted like every other piece of technology. Part of our job is to be able to diagnose problems with the monitor, and not be led astray.

In "Reversals", Peter Canning writes about a case where the arm leads were put on reversed, and the rhythm looked like VT.

     "The only thing going for me is that he doesn't look like he is about to die. I did not expect to see a rhythm like this. I look at it closer…I have the left and right arms                 mixed up. That'll do it."

If what you see on the monitor is totally out of left field, you have be a critical thinker and ask whether something could be wrong with the data. It happens some times. Leads are switched, cables break. That's part of clinical judgment, and our responsibility when using technology. You've got to have your "Spidey Sense" working at all times.

The limitations, however, do not overshadow the fact that we are supposed to figure out what is going on with our patients, and the cardiac monitor can play a crucial role in doing that. 

I looked at many of the posts by Dr. Smith of Dr. Smith's ECG Blog looking for cases of "treat the patient not the monitor". Guess what I found? He actually uses the information on the monitor! 

Dr. Mattu recently had his 100th video case presentation at his video blog. 100 videos? Why in heavens name would he do that when he could have just 1!

         "This week, we have a very difficult case… squiggles here, some blipity-blips there… Oh hell with it, just look at your patient!"

That would be one short video series! In all seriousness, they present tough cases. Difficult ECGs. Why aren't they saying "Treat the patient not the monitor?

We (all of us) don't always like to hear it, but every time we throw our hands up and say "treat the patient not the monitor", it has more to do with our limitations than those of the monitor. It means, "help, I can't figure this thing out, so I'll just treat the patient until we get to the hospital". 

That's what we do when we can't figure out what is going on. All of us.

Just know what it means when you do that. There was something on the monitor that you couldn't interpret. It is an opportunity to learn. That's what ems12lead.com is here for, and what other ECG blogs are here for as well.

"Treat the patient and the monitor".

Remember, it's all about the context!

As always, your comments are welcome!

 

 

 

 

 

 

Posted by on August 6, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , ,

49 Year Old Male: Chest Pain

25 comments

 

This excellent case comes to us from our friends in the UK. The author wishes to remain anonymous, but we thank him for his contribution.

It is about 8am on a gorgeous Wednesday morning, when your Paramedic unit is dispatched to a 49 year old male, "chest pain".

You arrive at the bungalow of a summer resort and are greeted by an elderly couple.

"They don't look too bad", you think, but you are not that lucky.

"Our son has been complaining of chest pain and vomiting for a couple of days".

You are led back to a room where you find your 49 year old patient lying in bed.

His parents say they found him like this and called 911. They tell you he seemed ok when he went to bed last night.

Your patient is lying supine in bed, responds to verbal stimuli only, and it is difficult for you to make sense of his answers.

You note that he appears anxious and uncomfortable, with dried vomit on his shirt.

His airway seems clear, but his respirations seem quick and a bit shallow, although clear bilaterally. You put him on a non-rebreather.

The rest of the vitals are as follows:

  • Pulse: 85 and regular
  • RR: 27, shallow
  • BP: 86/62
  • Pupils: equal and reactive
  • Skin: cool and slightly diaphoretic

While he is not adequately answering your questions, you are able to determine from his parents that he is an insulin dependent diabetic. You are unable to determine any other past medical history, medications, or allergies.

You check his blood glucose while your partner puts him on the monitor. The BGL reads "High". 

Here is the 12 lead:

 

 

You are 15 minutes from the local community hospital, and 30 minutes to the PCI center by ground. Air transport to PCI is a possibility.

 

What's your differential diagnosis?

What does the ECG show?

What do you want to do about it?

 

 

 

 

Posted by on July 22, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , ,

RBBB Abnormalities Missed

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The original presentation of this case appeared as  "What's Wrong with Mr. Wilson?"… You can read the original post here.

Much has been written lately about RBBB abnormalities that were missed. 

Dr. Smith has recently posted two cases here, and here discussing this.

First, let's review the 12 lead of a typical RBBB. When learning to recognize abnormalities, we must first be intimately familiar with what "normal" looks like. 

Editors note: Some astute readers may notice some subtle abnormalities of the ST segments here (so technically, not a normal ECG). I use this example to illustrate typical morphologies of the QRS complex:

                                                                                                                                            *image credit LITFL

 

Typical features of an uncomplicated RBBB:

  • Widened QRS of at least 120 ms
  • rSR' in V1-V3
  • Widened S wave in the lateral leads, most notably in leads I and aVL
  • Should follow the rule of "appropriate discordance" (if you are unfamiliar with this rule, refer to this previous post: Right Bundle Branch Block–Part II

Instead of the typical rSR' pattern in V1, you may in fact see any of the following morphologies:

It is not abnormal to have a small amount of discordant ST depression in the right precordial leads. However, ST elevation in the right precordial leads is never normal. In fact, the ST segments should not be distorted enough in RBBB to cause ST elevation at all. This is precisely why RBBB does not confound STEMI interpretation in the way that LBBB does, where ST elevation may be a normal finding.

Now let's take a look at the 12 lead of our 57 year old male patient who complained of feeling "really sick":

 

ECG findings:

  • There is sinus rhythm at a rate of about 80 bpm, with RBBB
  • Left axis deviation (bi-fasicular block)
  • Abnormally upright T waves in V1-V3
  • Questionable T wave in lead I
  • Slight elevation of the ST segment in V1-V2
  • Significant abnormal Q waves in V1-V4 with loss of initial R wave 

Overall, this is an ugly ECG. There should never be any ST elevation, and certainly the Q waves in V1-V3 are very abnormal and significant.

If we look at a normal RBBB and our patient's ECG side by side, the abnormalities become obvious:

From the previously mentioned RBBB posts by Dr. Stephen Smith (links above):

  • RBBB should not have ST elevation at baseline.
  • In RBBB, there should be some ST depression in V2 and V3. An isoelectric ST segment may represent relative ST elevation.
  • The presence of such well developed anterior Q waves suggest completed transmural STEMI.

Dr. Smith elaborates further on the Q waves:

"The wide Q waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle). This was common before the days of reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy"

The story of our patient:

The ECG recorded above was taken at admission to the cath lab. He was found to have a 99% lesion of his LAD. His ejection fraction was in the 30s.

He received a stent and a balloon pump, and was admitted to the ICU. His prognosis questionable.

Two weeks prior, he had started to feel very short of breath, along with a cough. On exertion, he felt "much more tired than normal".

After a few days he went to his PCP. His hx was significant for hypertension and smoking. It is unknown whether or not an ECG was acquired at that time.. He was, however, diagnosed with an URI and sent home with antibiotics.

He started to feel slightly better after a day or two, then began to decline again. He found himself without the energy to walk across the room. He had his wife drive him to the ED.

At the ED, they found him to be hypotensive (86/58) and not improving after the antibiotics. An ECG very similar to the one recorded above was acquired. Although it was not found to be diagnostic, there was concern that his issues could be cardiac. He was scheduled for a non-emergent cath a few days later.

At that time, the above ECG was acquired and the lesion was found.

KEY POINTS:

  • ECG abnormalities can be missed at many levels of care.
  • Become the "expert"– you can save lives!
  • You can not discover an abnormality until you are crystal clear on what "normal" looks like
  • Missed abnormalities can lead to delays in much needed patient care and possibly worsened outcomes

For more information, be sure to read our series on RBBB:

Right Bundle Branch Block–Part I

Right Bundle Branch Block–Part II

Right Bundle Branch Block–Part III

 

Posted by on July 13, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, training-development • Tagged: , , , , , , ,

77 year old female CC: Abdominal Pain

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It's a quiet Sunday afternoon when you're dispatched to a residence for a 77 year old female complaining of abdominal pain. Your dispatch notes indicates she was at the ED the day prior. Upon your arrival, you're met on the porch by the patient's son who directs you inside.

Your patient is sitting in a recliner, with mild respiratory distress, clutching her abdomen. Her skin appears a bit moist, and is warm when you touch her arm to feel for a radial pulse. When you ask her what is going on, she simply replies, "my belly won't stop hurting."

Your partner makes quick work of her vitals while you get the run down on her history.

  • Signs/symptoms: 7 of 10 abdominal pain going to her back, belching, intermittent vomiting
  • Alergies: Codeine
  • Medications: lisinopril, metoprolol, furosemide, potassium chloride, magnesium oxide, lipitor, albuterol, vitamin supplements, metformin, iron
  • PMHx: renal failure with dialysis (shunt Rt arm), hypertension, hypercholesterolemia, type II diabetes, pacemaker, asthma
  • Last ins/outs: vomiting x 3 today, did not do dialysis on Friday due to nausea/vomiting
  • Events: progressive worsening of pain and nausea

Your general impression of the patient is she just looks unwell. Your partner relays her vitals.

  • Pulse: 80 bpm, irregular
  • BP: 210/100
  • RR: 24, wheezes
  • SpO2: 94% on room air
  • T: 99.1 F (37.3 C)
  • BGL: 194 mg/dL (10.7 mmol/L)

Her son asks that you take her to the smaller, local hospital so, "she does not have to wait as long as she did at the ED yesterday." When you ask for her discharge instructions, he can only find the sheet which says Chest Pain and very generic information.

When you ask about her pain earlier, she denied any chest pain, however, to be prudent you obtain a 12-Lead:

Up and Down We Go - 12-Lead

You assist her to your stretcher, securing her with seat belts, and begin moving her to the truck.

  • What does this patient's 12-Lead ECG show?
  • What is this patient's rhythm?
  • What are your treatment priorities?
  • Can you still take this patient to a community hospital?

 

Posted by on June 11, 2013 • Filed under: ems-topics, patient-management • Tagged: , , , ,

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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Podcast: Play in new window | Download

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?”

15 comments

 

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: , , , , , , ,

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

5 comments

Happy New Year everybody!

We start 2013 with a continuation of our discussion about the field treatment of hyperkalemia. 

It might be helpful to review the first part of the discussion," HyperK and Shades of Grey" here. 

We are fortunate to have as a guest contributor Dr. Brooks Walsh of the Mill Hill Ave Command blog. An advocate of prehospital medicine, Dr. Walsh offers shares "Myths and Facts" of hyperkalemia with us. My sincerest thanks him for his valued contributions! 

I asked Dr. Walsh why he thought hyperkalemia presented such a challenge for EMS providers. Here is what he had to say:

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

But rather than curse the darkness, I wanted to go over some newer perspectives on hyperkalemia. Now, I don't want to simply reiterate all the great material that Dr. Weingart talked about on EMCRIT, so you really ought to download his great podcasts on the treatment of hyperkalemia and on why Kayexalate is likely ineffective, if not outright dangerous. The podcasts are real short, so just play them right now.

With that said, I'd like to review a few topics in hyperkalemia that deserve more attention:

 

Myth: Dialysis patients tolerate hyperkalemia better than other people.

Medicine is funny. I mean, there are "facts" that "everyone knows," but that are surprisingly hard to prove in studies. This is sort of one of those kind of facts, with very little evidence, and plenty of "real world" experience. Should we continue to believe it?

Maybe. It kind of depends on what we mean by "tolerate." If we mean "don't show ECG signs of hyperkalemia," then maybe dialysis patients do "tolerate" hyperkalemia better than other people. 

It's kind of hard to answer this definitively, though, since ECG signs of hyperkalemia, especially in the moderate range (e.g. < 6.5), are often absent on the ECG on all patients. We just don't see that many patients, dialysis or no, with severe hyperkalemia. Even in a study that looked only at dialysis patients, the vast majority had a K < 5.2, and ECG changes were accordingly infrequent.

But it may also be that dialysis patients, in fact, do show fewer signs of hyperkalemia on the ECG than do other people. A study done back in 1967 looked at dogs that received IV potassium slowly or quickly (but ending up at the same blood level). The faster infusions caused more ECG and hemodynamic effects. It is possible that ESRD patients, with a presumably slow increase in potassium levels, show fewer ECG changes than, say, a patient with acute rhabdomyolysis.

But the ability to avoid ECG changes isn't the "tolerance" we care about in hyperkalemia - we really care about the potential for patients to go into cardiac arrest. Hyperkalemia, regardless of ECG signs, puts the patient at risk for fatal arrhythmias. If you have either lab results or ECG evidence of hyperkalemia, that patient needs to be treated immediately – on that, most experts agree. I couldn't find any mention in the literature that suggests otherwise. For example:

                   "We emphasize that despite the absence of ECG changes of hyperkalaemia in ESRD, hyperkalaemia is still a     potentially life-threatening condition." –Aslam 2002

Or

"Some experts advocate calcium administration in patients whose serum potassium is >6.0–6.5 mm, even in the absence of EKG changes." –Putcha 2007 

 

Myth: If the ECG doesn't show QRS widening, then the patient is at low risk.

Some clinicians are under the impression that you can wait to treat the hyperkalemia until the QRS is "incredibly widened," showing huge sine-waves.  An ECG that shows "just T-waves" is presumably at lower risk, in this view.

Except that's not how it works, according to the experts. As these nephrologists explain:

                 "Five medical textbooks (two nephrology, two internal medicine, and one emergency medicine) advocate calcium gluconate in all hyperkalemic patients with EKG changes. "

Or this critical-care nephrologist:

                "It is apparent that neither the EKG nor the [potassium level] alone is an adequate index of the urgency of hyperkalemia,… hyperkalemia should be treated emergently for 1) K > 6.5 mmol/L or 2) EKG manifestations of hyperkalemia regardless of the [level]." –Weisberg 2008 "Management of severe hyperkalemia"

We asked Dr. Smith about his experiences with this topic, whether he has seen patients arrest without going through the ECG transition to widened, sine wave ECGs. His response as well was that "I have seen v-fib with peaked T waves only" on the ECG.

Stay tuned for "Myths and Facts Part II"!

 

Posted by on December 31, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

2013 STEMI Guidelines: EMS is Accountable

11 comments

On Monday, the American College of Cardiology Foundation and the American Heart Association released the 2013 Guidelines for the Management of ST-Elevation Myocardial Infarction. Their last updates to these guidelines were in 2004 and 2006, so this is an important milestone.

If you have been following our blog and podcast, most of the changes will not be earth shattering. We have long been advocates of evidence based STEMI care, which has put us at the bleeding edge as the guidelines take time to catch up. What does this mean for you, our readers?

Our readers have been ahead of the game! We're constantly impressed by your breadth and depth of knowledge.

The 2013 guidelines makes these changes, which we've covered before, to the identification of STEMI:

The honest answer is we probably would not have written a post about these guidelines if it were not for the following gem, buried on page 10 in the section on Regional Systems of Care (emphasis mine):

"For patients who call 9-1-1, direct care begins with FMC, defined as the time at which the EMS provider arrives at the patient’s side. EMS personnel should be accountable for obtaining a prehospital ECG, making the diagnosis, activating the system, and deciding whether to transport the patient to a PCI-capable or non–PCI capable hospital."

Folks, a joint task force of cardiologists has just placed the responsibility for the diagnosis and activation of a STEMI in the hands of EMS providers!

Many systems are already ahead of the game when it comes to STEMI care, but others lag behind.

We've taken responsibility for the care of cardiac arrest victims and now is the time we acknowledge the critical role we play in STEMI care.

  • Does your system acknowledege paramedic diagnosis of STEMI?
  • Are you ready to take on the responsibility of diagnosis and activation of STEMI?
Posted by on December 20, 2012 • Filed under: ems-topics, patient-management, Training • Tagged: , , , , , , , ,

Hyper-K and Shades of Grey

40 comments

Good morning all…

It's a beautiful fall Sunday morning, and you and your partner are enjoying an nice cup of coffee. But of course, the tones go off, and you are called to the residence of a 52 year old female, "sick". You recognize the address, you've been there before. 

Upon your arrival, you find your patient sitting in a chair in the living room. You remember her. She is a dialysis patient. She does not look well. 

She complains of not feeling well. She says she is weak, and has slight shortness of breath. You don't see any labored breathing or accessory muscle use, and she is able to speak in full sentences for now. Her respiratory rate seems ok, as does her pulse.

As you are getting your history, your partner gets a set of vitals. 

She tells you that she wasn't feeling great yesterday, and missed her scheduled Saturday dialysis (she is on a Tues-Thurs-Sat schedule). 

She thought she would be ok until Tuesday, but it didn't work out that way. She woke up today feeling really rotten and has been progressively feeling worse.

In addition to her renal failure, she also has a history of hypertension and asthma. She has no allergies. She says she has been compliant with her meds, and denies any chest pain or other aches/pains.

Her vitals are as follows:

  • HR         78 regular
  • BP         158/94
  • RR         20
  • SpO2     94 on room air
  • Lungs    very slight expiratory wheezes, but she states she always has that
  • Skin       unremarkable

You acquire an ECG that looks similar to this one:

image credit

You begin packaging your patient.

You are 20 minutes from the closet community hospital.

 

TODAY'S MISSION:

I am assuming most of you will recognize the above condition and know the available treatments for it. 

So, that is not the question.

The questions are these:

Do we treat this patient prehospitally? 

To be clear, the question is not "could we" but "should we"?

If we did, What would we use and why?

Is there a benefit to treating in the field versus waiting to hospital arrival?

 

**There is no obvious "right" answer to this… So, let's discuss it and see where we get. Have at it folks!

 

Posted by on November 30, 2012 • Filed under: ems-topics, patient-management, Training, training-development • Tagged: , , , ,

53 Year Old Male: Severe Leg Pain–Conclusion

5 comments

This is the conclusion to 53 year old male: Severe leg pain. You may wish to review the case.

Before we begin, my apologies for the delay in posting this conclusion. I live in coastal NY, and we got hammered by Hurricane Sandy. It has taken me a little time to get all caught up.

This is not an easy case. Our patient's chief complaint is of sudden onset of severe leg pain, and chest pain. Also notable is the measured hypertension.

Here is another look at the second 12 lead, which showed the following changes from the first:

There is sinus tachycardia, at a rate slightly above 100 bpm. There is physiologic left axis deviation. There are no signs of chamber enlargement, and the QRS is normal width. There is slight ST elevations in I and aVL, with ST depressions in the inferior leads, as well as V2 and V3.

At this point, our list of DDX should probably include:

  • DVT
  • Possible aortic dissection
  • STEMI

The patient's complaint sounds like it could be DVT, as many readers pointed out. We might expect to see swelling and redness as well, and this was not noted by the EMS crew. These signs and symptoms are not sensitive, however, as about 50% of people with DVTs will not have them. 

The patient is hypertensive, with chest pain, which led some of you to suggest an aortic dissection. Usually there is sudden onset of maximal chest pain, 10/10, with a "ripping" or "tearing" sensation. We do not have those typical signs and symptoms here by history. 

The patient does have ischemic signs on the 12 lead, consistent with lateral STEMI, but the patient's main complaint seems to be leg pain, not the chest pain.

 

So, how do we manage this patient? 

 

For starters, I think this is a tough patient to figure out. We have three good possibilities on our list of DDX, and two of them are immediately life threatening. 

I look at it this way, and of course it is with the benefit of hindsight. There seems to be more going on here than DVT, based on the patient's presentation, chest pain and 12 lead ECG. 

STEMI seems to be a reasonable assumption based on the 12 lead, but I would be thinking that as an atypical presentation (leg pain), this would almost be off the charts. It just doesn't seem like STEMI.

We also know that other conditions can cause ischemic changes on the ECG, and a dissecting aorta is one of them. 

Of course, O2 and IV access are indicated. NTG is a good possibility because it would be beneficial in either scenario. 

With that in mind, I would at least make sure we are transporting the patient to a hospital that can handle both STEMI and surgery for dissecting aorta. 

If a dissection progresses in a retrograde direction towards the aortic root, an acute total or partial occlusion of one of the main coronary arteries can occur. Usually, it is the RCA that is involved, but unusually, it can involve the left main. In the ED, heart rate and blood pressure will be controlled until surgery is performed. You can read more about this phenomenon here. 

As you have probably surmised by now, this was the fate of our patient. Once in the ED, a CT scan revealed a dissection of the ascending aorta. This dissection caused a partial occlusion of the LMCA. The patient underwent extensive surgery to repair the aorta. He was expected to make a strong recovery. 

We hope you enjoyed this unusual case! As always, comments are encouraged!

 

 

Posted by on November 26, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , ,

51 year old female CC: Near Syncopal Episode – Conclusion

7 comments

This is the conclusion to a 51 year old female CC: Near Syncopal Episode. If you haven't read the first part we highly recommend it!

When we left off, our crew was attending to a 51 year old female who had almost passed out in a stadium tunnel during a college football game. We received a few questions as to the type of football, which could be important to the diagnosis, so we will clarify that this was an American Football game.

Our crew had found her to be hypotensive, first bradycardic and then tachycardic, with concerning changes on the 12-Lead.  A nasal cannula at 4 L/min was initiated and they established bilateral IV's and were rapidly infusing nomal saline to restore perfusion.

Let's take a look at the initial rhythm strip:

Wouldn't Want to Miss the Big Game - Initial Rhythm

The initial rhythm strip shows a narrow complex tachycardia at ~130 bpm, without clear P-waves. Retrograde P-waves can be seen in numerous complexes T-waves, leading to a presumptive diagnosis of a junctional tachycardia.

Wouldn't Want to Miss the Big Game - Long Rhythm Strip

The longer rhythm strip shows sinus complexes followed by runs of junctional tachycardia. Astute readers will note Wenckebach conduction of the retrograde P-waves!

This finding alone would be highly concerning given our patient's present condition and history, however, when we move onto the 12-Lead her diagnosis is clinched:

Wouldn't Want to Miss the Big Game - Initial 12-Lead

The initial 12-Lead ECG again shows a junctional tachycardia, with markedly hyperacute T-waves and ST-elevation in the anterior precordials with downsloping ST-depression in the inferior leads. The degree of which the T-waves tower over the R-waves in V4 is truely impressive!

The crew immediately recognized the extensive anterior wall infarct with cardiogenic shock, and given the concurrent finding of a junctional tachycardia presumed there to be gross insult to the AV nodal tissue. They placed defibrillation pads on the patient and helped the arriving crew package the patient. The patient was able to follow commands and 324 mg aspirin was given PO. After 1 liter of fluid the patient remained hypotensive and another bolus was started. Oxygen was titrated to maintain an SpO2 of >96%.

Eventually the patient stated she had some dull pressure in her chest, but otherwise denied pain or shortness of breath. An early STEMI notification was given and while enroute to a STEMI receiving center the crew ran multiple 12-Leads, capturing the evolution of the myocardial infarction.

Wouldn't Want to Miss the Big Game - Subsequent 12-Lead 1

In this 12-Lead we can clearly see periods of alternating tachycardia and bradycardia, an ominous sign given the evolving MI. V5 and V6 were removed and adjusted closer to V4 and V7 so that defibrillation pads could be placed.

Wouldn't Want to Miss the Big Game - Subsequent 12-Lead 2

Wouldn't Want to Miss the Big Game - Subsequent 12-Lead 3

Wouldn't Want to Miss the Big Game - Subsequent 12-Lead 4

The patient was taken directly to a cath lab suite and found to have a 100% occlusion of the LAD and after the placement of a stent the patient's ECG normalized and her hypotension resolved.

This case illustrates the amazing evolution of an extensive anterior myocardial infarction and highlights the role the LAD can play in AV nodal function. We hope you enjoyed these ECG's as much as we did!

Posted by on November 18, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

51 year old female CC: Near Syncopal Episode

36 comments

This case comes from a reader who wishes to remain anonymous, as always details have been changed to protect patient and provider privacy.

You're working an overtime shift at a college football game on a hot Saturday in August, when a man flags down your crew. You head on over and are directed into one of the stadium tunnels to a female laying on the ground with bystanders pouring cold water onto her.

One of her friends reports she felt hot and dizzy while watching the game and came into the tunnel to, "cool off." She then said she felt faint and her legs gave out from underneath her and she fell to the ground.

You introduce yourself and ask the patient how she feels, however, while her eyes track you appropriately she is very lethargic and slow to answer. Her friends are unaware of any medical problems your patient may have.

Your partner obtains a set of vitals while you place the patient on the monitor.

  • LOC: alert to verbal (GCS E3 V5 M6)
  • Pulse: weak radials at 50 bpm
  • BP: 80/50
  • RR: 14, shallow, clear lung sounds
  • SpO2: 92% r/a
  • BGL: 68 mg/dL (3.8 mmol/L)

Your event jump bag lacks all but basic trauma and IV supplies so you request an ALS unit meet you on location. Your partner establishes an IV and hangs a bag of fluids. The rhythm strip prints out.

Wouldn't Want to Miss the Big Game - Initial Rhythm

Noting a difference in rate, you ask your partner to recheck her radial pulses. He confirms they are now at 120/min and weak; you direct him to place a BP cuff around the liter bag and to work on a second line.

Your partner asks, "should we give her anything for her blood sugar?"

A quick history from the patient reveals no major medical problems, takes no medications, has no allergies, and she denies any history of diabetes. You acquire a 12-Lead ECG as the ALS unit checks on scene.

Wouldn't Want to Miss the Big Game - Initial 12-Lead

Multiple rhythm changes are noted on the monitor and a long strip is printed.

Wouldn't Want to Miss the Big Game - Long Rhythm Strip

The ALS crew asks you for a report as you help place her on their stretcher.

  • What is your diagnosis? What are your next steps?
  • What does the first rhythm strip show?
  • What does the 12-Lead show?
  • What does the long rhythm strip show?
Posted by on November 11, 2012 • Filed under: ems-topics, patient-management • Tagged: , , ,