In case you missed it this week:
Have a great weekend!
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:
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:
- 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!
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.
- 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?
"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:
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!
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?
Summer is in full swing, and we are often asked about the best resources out there to learn more about ECG.
We decided to put together a list of "Editors' Picks" for some of our favorite "go-to" educational ECG resources.
Of course, this list is not comprehensive, and there are many outstanding books and sites that are not mentioned here this time around.
However, you have to start somewhere!
"12 Lead ECG: The Art of Interpretation" (Garcia and Holtz)
"Chou's Electrocardiography in Clinical Practice" (6th edition is recommended)
"Practical Electrocardiography" (Henry J.L. Marriott– Note: we recommend no later than the 8th edition– Marriott himself did not write later editions of the book)
"The ECG in Acute MI: An Evidence-Based Manual of Reperfusion Therapy" (Dr. Stephen Smith– Note: This book is solid gold, but very hard to come by since it went out of print.)
"Advanced ECG: Boards and Beyond" (Brendon Phibbs)
The World Wide Web:
Dr. Smith's ECG Blog– The Gold Standard
Life in the Fast Lane– The ECG Library is an invaluable resource
Dr. Amal Mattu's EKG Videos– Excellent weekly instructional videocasts
ECG Wave-Maven– Tons of practice ECGs to practice with from beginner to advanced. Detailed interpretations provided.
12 Lead ECG Challenge– Created by Tom Bouthillet
Editor's note: While listing the "12 Lead ECG Challenge" app could be seen as self-serving, I must tell you that this app is of such high quality and value that it simply can not be left off the list. I use it often. – David
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.
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":
- 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.
- 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:
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:
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?
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.