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47 year old male: Holiday Indigestion

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.

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.

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

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 Christopher Watford on January 24, 2013 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, data quality, EMS 12-Lead, Paramedic

“What’s wrong with Mr. Wilson?”

14 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 David Baumrind on January 19, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: 12-Lead ECG, case study, David Baumrind, ems12lead.com, Paramedic, respiratory distress

51 year old female CC: Near Syncopal Episode – Conclusion

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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:

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.

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:

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.

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.

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 Christopher Watford on November 18, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, acute anterior STEMI, case study, Christopher Watford, hyperacute T-waves, Junctional Rhythm, LAD occlusion, left anterior descending occlusion, Paramedic, STEMI

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.

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.

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

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 Christopher Watford on November 11, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, Paramedic

63 year old male CC: Substernal Chest Pain – Discussion

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This is the discussion for 63 year old male CC: Substernal Chest Pain, brought to you by Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. Be sure to review the first part!

When we last left off, our patient was a 63 year old male complaining of substernal chest pain which awoke him from sleep. We obtained standard, right-sided, and posterior ECG's which cardiology deemed non-specific. Our patient continued to have persistent chest pain even after maximal therapy.

Coronary catheterization was performed later that morning, and a total occlusion of the first obtuse marginal (OM1), a branch of the circumflex artery, was found. A drug eluting stent was placed, and his subsequent hospital course was unremarkable.

Could we have guessed this from the start? Let's take a look at his ECG's again:

Reviewing our patient's first ECG we see horizontal ST segment depression of 1 mm was seen in II and aVF, 3 mm ST depression in V2, and 1 mm ST depression in V3 and V4, all with upright T waves. An early R-wave transition was noted, with a height of 13 mV and an R/S of 1 in V2. Lead III showed T wave inversion.

The right-sided ECG featured only ST segment depression and inverted T-waves.

Reviewing the posterior leads, we see some interesting changes. Notably ST segment elevation of 0.5 mm in V7 and V8, and an unchanged appearance of the limb leads.

So, Dr. Walsh, what can we take away from this case?

Devoted readers of EMS 12-Lead will already know much about posterior MI, so I'll just do a brief review of the basics. I encourage you to search for the tag "posterior STEMI" for more information. As always, Dr. Stephen Smith's website also has plenty of examples and teaching about posterior MIs.

There is a small amount of controversy about what anatomic area of the heart a "posterior" MI actually affects. Some have suggested that the infarct is actually in the infero-basal region, while others have evidence that it should be viewed as a lateral infarct.

Regardless of the name, however, it generally is the result of an occlusion of the left circumflex coronary artery (link to cool animation). This territory is generally regarded as "electrically silent" in the standard ECG leads. As such, diagnosis relies on indirect evidence in the standard leads, as well as the use of non-standard "posterior" ECG leads.

So, how can we be Posterior STEMI Rock Stars, Doc?

For years, the standard teaching on identifying a posterior MI has emphasized some common elements. Brady summarized the most important of these:

Horizontal ST depression in V1-V4

Tall, broad R waves (>30ms)

Upright T waves

Dominant R wave (R/S ratio > 1) in V2

So, a typical posterior STEMI looks like this:

Inferioposterior STEMI courtesy of LifeInTheFastLane.

Note the ST elevations in the inferior and lateral leads; in general, a posterior MI usually shows signs of a STEMI in either of these two regions the majority of the time. It's pretty obvious that evidence of STEMI in one area (e.g. inferior) certainly strengthens suspicion for a posterior MI.

However, here's an example of a posterior MI that does not show any inferior or lateral involvement:

Posterior STEMI without inferiolateral changes. (PubMed)

Using posterior leads (V7-V9) can show ST elevation, but the magnitude may not be as dramatic as that seen in the "usual" STEMIs. Many experts consider, for example, 0.5 mm of elevation to be significant, instead of the usual > 1 mm criteria, and that elevation in just one lead is sufficient.

So what's wrong with the conventional thinking?

There's a short-cut way to diagnose a posterior MI, that involves "flipping" the ECG. The idea is that the ST depression in the anterior leads is a "mirror" view of ST elevation in the posterior wall, and that the tall R-waves are actually deep Q-waves.

For example, a blow-up of lead V2 from the isolated posterior MI above (the second ECG) looks like this:

It fulfills all the criteria I reviewed above, so it's a classic example of how we currently define a posterior MI. And if we "flip" it, we get this:

Yep Doc, that looks like a regular STEMI now!

For many people (MDs included!), the diagnosis of a posterior MI starts, and ends, with this flipping.

I'll tell you what has always bothered me though. Look at the R-wave in the un-flipped image. This is just the mirror image of the Q-wave, and our "flipped" image reinforces that. In fact, the Q-wave in our flipped image looks pretty darn old, like the MI has progressed far along already.

Furthermore, the T-wave in our "flipped" image hardly looks hyper-acute. In fact, it looks like the T-waves are in the process of returning to baseline, another indication that our "classic" posterior MI is old.

Here's an example of an subacute/old inferior MI, for comparison. Also note the resolving, partially inverted, T-waves in III and aVF:

Old Inferior MI courtesy of LifeInTheFastLane.

It looks instead like our description of posterior MI is training us to look for old, completed MIs!

Let's look at this from another angle. Look at this typical inferior STEMI, and focus on lead aVF:

That's a classic STEMI, no doubt. Tiny Q-waves, tall T-wave – everything suggests that this is very acute.

Now, instead of being lead aVF, let's pretend it were lead V9. What would the "flipped" view of this lead be? Let's flip it and see!

This view shows a small R-wave, and a fully inverted and deep T-wave. Now, if we take a look back at the criteria listed above for a posterior MI, however, it would not meet much of the description of a posterior MI we listed before.

We're teaching people to pick up on old posterior MIs, and training them to miss the acute presentations.

Interesting, so how can we avoid this, Doc?

Well, I may have had this thought kicking around in my head, but some cardiologists actually wrote down these thoughts! Birnbaum et al. just published the article Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. This wasn't a prospective controlled trial, but they managed to get 13 cardiologists to agree on a few things.

One of those was that our standard description of the morphology of posterior MI on the ECG is likely wrong. Helpfully, they proceed to describe what we ought to be looking for!

After reviewing the usual evolution of LCx-occlusion MI, they conclude that the standard definition, that relies on tall R-waves and upright T-waves is:

… the late “mirror image” of fully evolved ST-segment MI (STEMI) (Q waves with terminal T-wave inversion) and not the acute phase of STEMI.

By contrast, they give an example of what they consider to be an acute posterior STEMI:

If we blow up lead V2…

…we see that there is a small R-wave, and fully inverted T-waves, and an R/S < 1. It meets none of Brady's criteria above. But if we flip it…

It looks like a regular ol' STEMI!

Bring it home for us, doc.

The usual description of posterior MI may be in need of revision. The posterior leads, however, remain useful to reveal acute cardiac ischemia.

Thank you again to Dr. Brooks Walsh for this case and his insight into posterior STEMI!

Did you catch the posterior STEMI?
Does your service allow you to activate a posterior STEMI?

Posted by Christopher Watford on November 2, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, acute posterior STEMI, Brooks Walsh M.D., case study, Christopher Watford, posterior leads, posterior STEMI, right sided leads, STEMI

24 year old male: “Anxiety Attack” – Conclusion

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This is the conclusion to our case 24 year old male: "Anxiety Attack". Be sure to read Part I before the conclusion!

When we left off, our providers were on scene with a young man, in custody, who was pale and had a radial pulse too fast to count. A narrow complex tachycardia was present on the monitor to which our patient helpfully pointed out, "it's SVT".

Let's find out if our patient is right!

The initial rhythm strip shows a regular, narrow complex tachycardia at approximately 200 bpm. Differentials include SVT (e.g. AV Nodal Reentrant Tachycardia and Orthodromic AV ReciprocatingTachycardia), atrial tachycardia, atrial flutter, and atrial fibrillation. However, given the rate, it would seem unlikely to be flutter, and given the near dead-on regularity it excludes atrial fibrillation.

The 12-Lead ECG confirms much of what we saw in the initial rhythm strip. We have a regular, narrow complex rhythm at 200 bpm. Retrograde P-waves are appreciable in leads II, III, aVF, and V1. These P-waves are often termed pseudo-S or pseudo-R' waves, and are most commonly seen in AVNRT. However, ST-elevation in aVR during SVT is a sign of orthodromic AVRT.

Regardless of mechanism, it is safe to say that our patient was right! He is currently experiencing SVT.

The treating paramedic also came to this conclusion and began treatment by lying the patient down and attempting vagal maneuvers. The patient was coached to bear down and then to blow through an empty 10 cc syringe, both without effect:

An 18 gauge IV was established in the left antecubital fossa. 6 mg of adenosine was then administered rapid IV push followed by a 20 cc normal saline bolus flush. The following was captured:

This rhythm strip shows an interruption in the AV nodal reentry circuit with a conversion to a sinus tachycardia.

A repeat 12-Lead was obtained by the crew:

The post-conversion 12-Lead shows a sinus rhythm without delta waves, epsilon waves, or acute ST/T-wave changes. The computerized interpretation notes a short PR interval of 98 ms, however, this author reads the PRi as normal at ~120ms. If an accessory pathway is present, conduction is concealed on the patient's baseline 12-Lead.

The patient was transported by the crew without incident and was lost to follow-up by EMS. However, this case shows that sometimes our patients will know exactly what is wrong, which underscores the importance of obtaining a good history.

What conditions could this patient have which caused his SVT?
What treatments may this patient receive if he continues to suffer from SVT?

Posted by Christopher Watford on October 8, 2012 • Filed under: ems-topics, patient-management • Tagged: adenosine, case study, Christopher Watford, EMS 12-Lead, narrow complex tachyardias, Paramedic, Prehospital 12-Lead ECG blog, treating SVT with adenosine

62 year old male: Chest Discomfort – Conclusion

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This is the conclusion to our three part case series, 62 year old male: Chest Discomfort. Before reading the conclusion, we suggest you check out Part I and Part II. Thanks again to Vince DiGiulio, EMT-CC for this wonderful case!

When we last left off, our patient had experienced a resolution of his chest pain accompanied by changes on his 12-Lead ECG. The ED physician had called cardiology, but they were unimpressed. Are we comfortable with this?

Let's review our patients' first 12-Lead.

We have a narrow complex, regular rhythm at 90 bpm consistent with a normal sinus rhythm. Flat or downsloping ST segments are visible in leads III and aVF. Additionally, ST-Elevation is present in leads V1 through V4. As some readers pointed out, this is diagnostic for an Anterior Wall Myocardial Infarction. There are also some subtle hints that this is not a normal variant:

Dr. Smith included in the comments that the R-wave amplitude of V2-V4 is only 10 mm. In cases of AWMI, a loss of precordial R-wave amplitude is often noted.
If you compare the T-waves in V1 and V6, you'll note that they are much larger in V1 than in V6. Dr. Henry J. L. Marriott describes this finding as a "loss of precordial T-wave balance." Dr. Mattu covers this in depth in his excellent video New Tall T-Waves in V1.

The most important point is that there is no other explanation for our patient's ST-Elevation. There is no LVH or BBB present and Early Repolarization is a diagnosis of exclusion in a 62 year old patient.

Regardless, any patient with chest pain should be evaluated with serial ECG's. During our patient's second 12-Lead, he happened to be pain free:

Our repeat 12-Lead shows a normal sinus rhythm, with the development of terminal T-wave inversions in leads V1-V4. Several of our readers correctly pointed out that these are the hallmarks of the eponymous Wellens' Syndrome (or Wellens' Warning). Interestingly enough, the computer's interpretation now displays *** ACUTE MI ***.

So what is the importance of this finding?

In 1982, Hein JJ Wellens identified two types of abnormal T-waves associated with critical, proximal LAD stenosis. The first type, not seen in our case, features deeply inverted, symmetric T-waves in the anterior precordial leads. The second type, featured above, are characterized by biphasic T-waves. In his seminal study, Wellens found that these electrocardiographic patterns were most often seen during pain free periods. Subsequent studies showed that nearly every patient with Wellens' Syndrome had blockage in the LAD, ranging from 50-100%!

So what happened with our patient?

Our patient continued to experience transient episodes of chest pain. His troponin-I levels returned at 1.09 ng/mL 20 minutes after the pain-free ECG. Recognizing Wellens' Syndrome, the ED physician had the patient transferred directly to the cath lab for immediate PCI.

Key points highlighted by this case:

Obtain Serial ECG's!
A single ECG diagnostic for STEMI is indication for cath lab activation.
Resolution of chest pain is not a reason to withold aspirin.
Wellens' Sydrome strongly suggests an advanced degree of LAD stenosis and requires urgent evaluation.

References

Dr. Smith's ECG Blog – Wellens' Syndrome
de Zwann C, Bar FW, Wellens HJJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982; 103:730-736. [PubMed]
Parikh KS, Agarwal R, Mehrota AK, Swamy RS. Wellens syndrome: a life-saving diagnosis. Am J Emerg Med 2012; 30:255e3-255e5. [PubMed]
Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med 2002; 20(7):638-43. [PubMed]

Posted by Christopher Watford on October 5, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, acute anterior STEMI, acute anterior STEMI vs. benign early repolarization, case study, Christopher Watford, EMS 12-Lead, serial ECGs, Wellens' Syndrome

24 year old male: “Anxiety Attack”

23 comments

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

You're dispatched on an ALS quick response vehicle by law enforcement requesting EMS to check up on a subject. Dispatch notes indicate officers were called reference a domestic disturbance and have two subjects in custody. A BLS ambulance just around the corner from the call checks on scene and requests ALS continue.

You're directed into a small apartment by an officer and find the BLS crew obtaining vitals from a young man, who appears pale, seated on a couch, uncuffed. The officer says, "he started complaining of chest pain and his hands tingling after we arrested him, might be an anxiety attack. He and his girlfriend really got into it."

You check in with the BLS crew who are obtaining his vitals and introduce yourself to the patient. He looks up at you and simply states, "It's SVT."

One of the crew looks up and nods his head while giving the vitals:

Pulse: too fast to count
BP: 118/64
Resps: 18, unlabored
SpO2: 94% r/a, cap refill normal
JVD: moderately elevated

A quick assessment is made:

Signs and Symptoms: Palpitations and SOB
Allergies: None
Medications: None
PMHx: "I've had SVT a lot, like twice already this month."
Last In's and Out's: Dinner
Events: verbal altercation with girlfriend

During your exam the BLS crew has placed the patient on the monitor for you:

As it prints out, you tell one of the officers that he's definitely a patient and will be going with you to the hospital.

A 12-Lead is acquired:

Is this patient actually in SVT?
What is your treatment plan?
What sort of medical problems could this patient have?

Posted by Christopher Watford on October 4, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, EMS 12-Lead, ems12lead.com, narrow complex tachyardias, Paramedic

62 year old male: Chest Discomfort – Part II

8 comments

This is part two of the three part series, 62 year old male: Chest Discomfort. As before, clinical details have been altered for educational purposes and to protect patient and provider privacy.

When we left our patient, he was experiencing the latest in what had become a series of episodes of minor chest pressure. A 12-Lead was acquired, and is given below:

He looked pretty good, but as most of you noted, his ECG was at best borderline, and at worst, diagnostic of anterior STEMI. We'll hold off on our interpretation until the conclusion. So what happened next?

The tech who ran the ECG had the good sense to make this patient a priority and quickly got a physician to lay her eyes on the ECG. Like many of you, she was concerned about a STEMI, but not convinced. There was, however, one important thing she was sure of: even being suspicious of STEMI was cause enough to warrant expedited care.

The patient was immediately brought back to a room, placed on a nasal cannula at 2 L/min, and attached to the cardiac monitor while IV access was obtained and labs were drawn. The physician continued her evaluation and completed a thorough history and physical examination.

However, after leaving the room, she was torn. The patient had a history consistent with angina and a worrisome ECG, but during the previous activities his pain had disappeared yet again.

She put a page out to cardiology, but knew ahead of time that it was going to be a hard sell. It was evening and the facility where the patient presented did not have PCI capabilities on-site. Inter-facility transfer and calling in the cath-lab team would be an extra hurdle if she really wanted to push for that pathway.

When cardiology called back they didn't seem too anxious to come in right away. He didn't have any strong risk factors, the ECG sounded non-diagnostic over the phone, and he was now pain free. They would see the patient, but it would be on a non-urgent basis later in the evening.

So, worried there was more going on than stable angina, the treating physician ordered a repeat ECG. The timing was just about 30 minutes after the first, lead placement was identical, and the patient was pain free without additional intervention:

What does the patient's 12-Lead show now?
This 12-Lead was acquired while the patient was pain free, are they in the clear?
What are your next steps for this patient?

Posted by Christopher Watford on September 30, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, Paramedic, Prehospital 12-Lead ECG blog

62 year old male: Chest Discomfort

20 comments

This another great case study from Vince DiGiulio, EMT-CC. As always, some details have been changed to protect patient privacy.

It's Monday night and you're working triage in a busy emergency department. The waiting room is full when a very pleasant 62 year-old man presents to the desk with a chief complaint of chest discomfort. You sit him down in a wheelchair while he gets registered and perform a quick "eyeball" examination.

The patient is a well-appearing middle-aged male in no acute distress, who actually appears younger than his stated age. He is alert, oriented, and answers all questions appropriately, with skin that is warm and dry and a strong radial pulse that's not too fast or too slow. His breathing is unlabored and he states that he has been experiencing some minor chest discomfort for around for two days.

You figure that he's not going to collapse in the lobby and leave to speak with the triage RN while he signs some paperwork. The two of you decide to bring him back to the dedicated ECG nook, where the nurse will perform a triage assessment while you obtain vitals and run a quick ECG.

Onset: 2 days ago
Provocation/Palliation: He cannot describe any provoking factors, but states "I usually rest and it eventually goes away"
Quality: Midsternal chest pressure
Radiation: None
Severity: "Not bad at all, maybe a 3 out of 10."
Timing: Intermittent, with spells lasting for 10 minutes or so and possibly increasing in duration more recently. The current episode has lasted at least 15 minutes.

Using an automated monitor, you obtain the following vitals:

Pulse: 92 bpm
BP: 147/88 on his left arm
Resps: 20, unlabored, and clear bilaterally
SpO2: 96% on room air
Temperature: 37.1 C (98.8 F) orally

At the same time, the nurse elicits the following information:

Signs/Symptoms: Intermittent midsternal chest pressure x 2 days. No diaphoresis, nausea, vomiting, SOB, or dizziness.
PMHx: No significant medical history besides well-controlled HTN and an appendectomy in his 20's
Meds: "some blood pressure medication"
Allergies: NKDA
Last In's/Out's: Dinner
Events: "This discomfort started a couple of days ago. It comes and goes, but my wife wanted me to get checked out and I finally gave in after dinner when it started to return."

You run the following 12-Lead:

There is no old ECG in your electronic medical record for comparison, and when you walk back to the main department, you cannot find a physician to look at the tracing. One is performing an I&D of a peritonsilar abscess, while the other is probably with a patient somewhere but MIA.

Every room is filled, most of the hallway beds are occupied, and there is certainly a line forming at the front desk while you're wandering around in back.

Are you concerned about this ECG?
Do you need to pull a physician away from someone else to look at it?
Does he need to jump to the front of the queue and get a room right away?
If you were in the field, how would you treat and transport this patient?

Posted by Christopher Watford on September 28, 2012 • Filed under: ems-topics, patient-management • Tagged: case study, Christopher Watford, EMS 12-Lead, Paramedic

57 year old male: Chest Discomfort – Conclusion

14 comments

This is the conclusion to 57 year old male: Chest Discomfort. We suggest you read the backstory first!

We're now in the back of the ambulance with our stubborn 57 year old male with a rapid heart rate. He looks unwell, but is otherwise hemodynamically stable. Our partner is working on a line.

Let's review the initial rhythm and 12-Lead ECG:

The rhythm strip shows a narrow complex tachycardia at approximately 150 bpm. Atrial activity is not visible and may be buried in the T-waves. Our differentials include: sinus tachycardia, supraventricular tachycardia (e.g. AV Nodal Reentry Tachycardia and orthodromic AV Reciprocating Tachycardia), 2:1 atrial flutter, and junctional tachycardia.

The 12-Lead also shows a narrow complex tachycardia at approximately 150 bpm. Atrial activity is vaguely appreciable in the T-waves of V1 and III. The list of differentials remains unchanged, however, given the continued regularity sinus tachycardia seems less likely.

The paramedic who sent this case in elected to treat the patient with adenosine to convert or unmask the underlying rhythm.

The post-adenosine rhythm strip shows clear flutter activity in leads II and aVF, however, the paramedic admits they did not initially notice the F-waves. The rhythm then devolved into an irregularly irregular rhythm and a strip was printed.

While there is some baseline wander present, given the previous ECG, it seems very likely that this is atrial flutter with a variable response. However, the rhythm quickly accelerated to its original rate of 150 bpm.

As the treating paramedic did not appreciate atrial flutter, they administered a second dose of adenosine.

Atrial flutter is readily appreciable in Leads II and aVF, and as before the rhythm accelerated to its original rate.

The treating paramedic recognized atrial flutter and contacted medical control asking for orders for Cardizem.

Orders were received for 10 mg Cardizem slow IV push, which resulted in some reduction in rate but without conversion to a sinus rhythm.

The patient was transported to a local hospital where he was placed on a Cardizem drip, resulting in conversion to a sinus rhythm after a few hours. A follow-up with a cardiologist was scheduled and the patient was discharged home without sequelae.

Any time you are faced with a regular rhythm at around 150 bpm, remember that the most common atrial rate in atrial flutter is 300 bpm and the most common conduction is 2:1.

For more tips to becoming an Atrial Flutter Rock Star, check out our friend Vince DiGiulio's blog post "Diagnosing Hidden Atrial Flutter".

Posted by Christopher Watford on September 21, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, atrial flutter, case study, Christopher Watford, EMS 12-Lead, narrow complex tachyardias, Paramedic, Prehospital 12-Lead ECG blog

59 Year Old Male–”Lifting Boxes”: Part II, with a twist!

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This is part II to 59 year old male–"Lifting Boxes". You may wish to review the case.

Let's review the ECG:

There is sinus rhythm at about 90 bpm. Some of you saw a slight bit of ST elevation in the inferior leads, and maybe an abnormal aVL. Perhaps? Perhaps not? V1-V4 look possibly abnormal, but there is an awful lot of artifact. There appears to be a bit of ST depression in V5-V6. Is this an ischemic ECG? Looks concerning from what we can decipher.

Sometimes on blog posts, we get used to crisp ECGs and tidy scenarios. Nothing wrong with that. Sometimes, though, our cases on the street just don't go like that. Often there is much to learn from those, but I digress.

There are a couple of real concerns with this case;

As correctly pointed out in the comments, the quality of the ECG is poor. This leads to all sorts of interpretation problems. If we put effort into it, we can usually get a pretty good tracing. On occasion though, it can be tough.

Another issue is that the 12 lead was not acquired early on. The crew acquired the ECG in the ambulance after the following: assessment, history, physical exam, O2, ASA, bathroom break, change of clothes, etc. This is not what we are after, and we could miss important findings by waiting this long.

As most of the comments reflect, the timing of the ECG and poor quality make it tough to interpret, and tough to activate the cath lab. I know some of you saw findings that led to you say you would activate, but doing so based on this one poor quality ECG is tough to do. Just is.

So off to the community hospital he went.

Calls are run like this every day. We all know it. In fact, it is one of the reasons we discuss cases such as this.

Could this patient have benefited if the call was handled differently?

Fortunately, we know that he did!

In a contrasting plot twist, this call was actually handled quite differently:

In reality the crew obtained the history and vitals previously mentioned. However, undaunted by the patient's reluctance they convinced him to allow a 12 lead to be acquired immediately. This is what they found:

Due to the patients girth and breathing patterns, it was difficult for the crew to acquire a totally clean ECG. However, this one clearly shows ST elevation inferiorly, as well as V5 and V6. We can also see ST depression in V2-V4 with tall R waves. There is also slight ST depression in aVL: Infero-postero-lateral STEMI.

The crew acquired another 12 lead with V4R which revealed about 1mm of ST depression in V4R:

The ECGs were transmitted, and the patient was emergently transported to the cath lab, where he underwent PCI and had a successful outcome.

For comparison, note how much the ST segments resolved from the first 12 lead to the one acquired in the ambulance:

After just a short period of time from the first ECG, obvious ST elevation in II and III has mostly resolved. Timing is everything!

The point of all of this is to clearly illustrate the importance of early 12 leads and good data quality. The prehospital care of this patient could have gone either way. We see it every day. How we handle those first minutes, and the quality of the data we acquire will have a huge impact on the care our patients receive.

What are your thoughts? I'm sure you have experiences similar to this one!

Posted by David Baumrind on September 20, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: 12-Lead ECG, case study, data quality, David Baumrind, ems12lead.com, inferior STEMI, Paramedic, serial ECGs, STEMI

57 year old male: Chest Discomfort

70 comments

The following is a great case from Mordy E, and as always some details have been changed to protect patient privacy.

You and your partner are refueling your ambulance at a gas station when a woman walks up and asks if you could, "come check out my husband."

As you walk over to their car she states that, "he's had chest pain for almost 5 hours now and didn't want me to call 911."

Your patient is standing, pumping gasoline, and appears unwell and diaphoretic. He seems reluctant to accept care at first, but you encourage him to let you check him out and he admits to chest discomfort.

He sits down in the passenger seat and lets you evaluate him.

Onset: 5 hours ago
Provocation/Palliation: nothing makes it better or worse
Quality: "pressure"
Radiation: "to my jaw"
Severity: "it isn't that bad"
Timing: constant

Your partner puts the monitor on the back seat and places electrodes while you get a set of vitals.

Pulse: 150, weak at the radials
BP: 102/68
Resps: 22, unlabored, clear bilaterally
SpO2: 94% r/a

As the initial rhythm strip prints and your partner places electrodes for a 12-Lead, you get a quick medical history.

PMHx: hypertension, hyperlipidemia, palpitations
Meds: "some pressure medication"
Allergies: seasonal allergies, NKDA
Last In's/Out's: breakfast
Events: sudden onset of chest discomfort which woke him up this morning

Your partner hands you the rhythm strip and leaves to grab the stretcher as the 12-Lead prints.

You tear off the 12-Lead and the patient asks, "well, is something wrong with my heart?"

Your partner places the stretcher in front of the patient and says, "yessir, your heart is going too fast. Let's get you on our cot and into the back of our office so we can do something about that."

As you wheel the patient to the unit, your partner asks:

What is our patient's rhythm?
What did the 12-Lead show?
How should we treat this patient?

Posted by Christopher Watford on September 18, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, EMS 12-Lead, narrow complex tachyardias, Paramedic

88 year old female: Weakness – Discussion

1 comment

This is the discussion for 88 year old female: Weakness. If you've not read the backstory, we suggest you check it out!

When we last left off, our patient was in an exam room with an irregularly irregular rhythm. The ED physician had asked you if the patient had a history of atrial fibrillation.

Let's review the rhythm strip and 12-Lead ECG.

We have a narrow complex, irregularly irregular rhythm at 70-110 bpm. There is no apparent atrial activity. This is presumably atrial fibrillation.

The 12-Lead ECG shows a narrow complex, irregulaly irregular rhythm with no acute changes to the ST-segments. What may be atrial activity is visible in multiple leads, however the baseline is variable. A diagnosis of atrial fibrillation cannot be ruled out, however, another atrial arrhythmia should be suspected.

When in doubt over atrial activity, the Lewis Lead can help you highlight it on the surface ECG (a tip of the hat to Kelly Grayson who first introduced me to this lead). All this requires is moving the RA and LA leads into position along the sterum like so:

To acquire a Lewis Lead, place the RA electrode on the manubrium and the LA electrode approximately where V3R would go and then monitor Lead I.

Once they acquired a strip from the Lewis Lead they were certain of the eventual diagnosis:

From the Lewis Lead strip we can easily appreciate at least 5 distinct P-wave morphologies! Therefore our patient is experiencing a multifocal atrial rhythm. For completeness, multifocal atrial rhythms with a normorcardic rate is referred to as Wandering Atrial Pacemaker, while a tachycardia rate is referred to as Multifocal Atrial Tachycardia. In either case, treatment is geared towards correcting the underlying problem rather than the rhythm.

So, what are some common causes of multifocal atrial arrhythmias?

Jason Roediger did our work for us in the comments and listed the major causes:

MAT is most commonly associated with chronic obstructive pulmonary disease (COPD) in addition to associated lung disorders: far-advanced pneumonia, chronic bronchitis, emphysema, etc. It can also be seen in digitalis intoxication as well as other diseased states.

Other causes include electrolyte disorders such as hypomagnesemia and hypokalemia or even theophylline usage can cause MAT.

In this case our patient was found to have a chest X-ray consistent with emphysema and cardiomegaly. Her labs were notable for a low chloride, bacteria in her urine, and an elevated white count. She was admitted for urosepsis and dehydration. On admission day two she was found to have a small bowel obstruction, however, after discussing treatment options with the patient and family she refused surgery and elected for comfort care only.

If our intrepid reader had not run the Lewis Leads in this case, the patient may have received antiarrhythmics and anticoagulation therapy for a new onset of atrial fibrillation. The key takeaway here is that not all irregularly irregular rhythms are atrial fibrillation!

Have you used the Lewis Lead to diagnose an arrhythmia? We'd like to know!
Check out Kelly Grayson's wonderful article The Leads Less Traveled for other novel lead placements.

Posted by Christopher Watford on September 14, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, EMS 12-Lead, irregular tachycardias, Lewis Lead, multifocal atrial tachycardia, Paramedic, Prehospital 12-Lead ECG blog

88 year old female: Weakness

17 comments

This great case was submitted by Vince DiGiulio, EMT-CC; we highly recommend you read his wonderful blog The Medial Approach to Emergency Medicine. As usual, the case has been altered to protect patient and provider privacy.

You're working triage in a busy urban ED when an 88 year old female is brought in by her family. She is in a wheelchair and appears lethargic.

When you introduce yourself she comes around and is able to answer your questions, albeit with some hesitation. Her family reports that she is independent and lively at baseline and are concerned she is having a stroke.

You move her into a triage room and grab a set of vitals. Her breathing appears unlabored with an irregularly irregular pulse at her radials. You ask an ED tech to join you to help with acquiring an ECG.

Pulse: 80-100, irregularly irregular
BP: 122/83, auto-cuff
Resps: 22, unlabored, clear bilaterally
SpO2: 92% r/a
GCS: 14 (E3 V5 M6)
LAPSS: Negative

The ED tech runs a strip from the monitor after switching to Lead I as Lead II had small complexes.

You call back to the charge nurse and ask for a bed assignment and wheel the patient back with the help of the ED tech. In the room a 12-Lead ECG is acquired while a complete history is gathered.

PMHx: hypertension, hypercholesterolemia, Type II diabetes
Meds: lisinopril, Lipitor, glipizide, ASA, and a multivitamin
Allergies: PCN and Sulfa
Last In's/Out's: normal lunch, vomiting during the afternoon
Events: progressive lethargy and weakness after vomiting in the afternoon

The RN hands you a copy of the 12-Lead while she updates the electronic chart.

Given the 12-Lead you decide that a Lewis Lead should be acquired, as it may give additional insight into the underlying rhythm:

The ED physician walks into the room and asks you one question, "does she has a history of atrial fibrillation?"

What is this patient's rhythm?
What are some potential causes of our patient's rhythm?
Does the Lewis Lead offer any potential insights into our pateint's rhythm?
Would this information change your treatment decision?

Posted by Christopher Watford on September 11, 2012 • Filed under: ems-health-safety, ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, irregular tachycardias, Paramedic, Prehospital 12-Lead ECG blog

Snapshot Discussion: 64 Year Old Male–Chest Pain

7 comments

This is the discussion for "Snapshot: 64 Year Old Male–Chest Pain".

First, let's talk about the patient presentation.What is concerning is the substernal chest pain, radiating to the shoulder and neck area. While this occurred about 30 minutes after exercise, it did not occur during exercise, so that is somewhat atypical. Still, enough red flags in the history to be very concerned.

Here is another look at the 12 lead:

It is a regular sinus rhythm, at a rate of 65. The PRI is on the long side of normal at 200 ms, and the QRS is slightly wide at just over 100 ms. The axis is normal, and there does not appear to be anything causing secondary ST changes.

The question is, do we see signs of ischemia on this ECG?

This is not an obvious ECG, so as we would expect, many of you said yes, and many said no. Is this a normal ECG? We don't have an old ECG for comparison, but I would say this ECG is not normal.

Let's break it down. What jumps out at me most on this ECG are the morphologies in leads I and aVL:

There is almost 1 mm of flat ST depression in lead I, and a very notable T wave inversion in aVL.

While the T waves look large in leads III and aVF relative to the size of the QRS, there appears to be no ST elevation at this time.

Dr. Stephen Smith, of the famed Dr. Smith's ECG Blog, has written numerous times that depression and/or T wave inversions in aVL will often precede ST elevation in the inferior leads in IWMI.

Also see this recent case by Dr. Amal Mattu for another case on this subject.

Are there any other findings on this ECG that might support these concerns?

There is about 1 mm of ST elevation in V1. Could there be RV involvement?

At the very least, I would be very concerned about a developing IWMI. The patient's discomfort is diminished, but not resolved. His complaints of "indigestion" are common with IWMI, and diaphoresis is another red flag.

Having said that, would I activate the cath lab based on this ECG? I have to say I would probably not activate based on this ECG alone.

I think this ECG is very concerning, but not yet diagnostic. I would certainly acquire serial ECGs and scrutinize the inferior leads for any subtle signs of change.

Dynamic changes would be a clincher. I would also treat with ASA and NTG, and would divert to PCI center if any changes in the ECG evolved.

This being a "Snapshot" case, we do not have follow up on this patient, or repeat ECGs.

We run into this in the field often. The spectrum of ACS is far and wide, and we are often presented with borderline ECGs.

I think the best course is to treat based on what is best for the patient, and do serial ECGs!

Thanks for all of the insightful comments on this case!

Any additional thoughts?

Posted by David Baumrind on August 24, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: 12-Lead ECG, case study, David Baumrind, ems12lead.com, IWMI, serial ECGs

77 year old female: Unresponsive – Discussion

11 comments

This is the discussion for 77 year old female: Unresponsive, if you have not read the case report we recommend you start there!

First, a hat tip to our readers who were unafraid to tackle this challenging scenario. Second, we were very impressed to see a number of readers correctly identify this challenging rhythm!

When we left off our crew was attending to an altered 77 year old female they picked up at a local skilled nursing facility. The patient's presentation seemed fairly routine for an Altered Mental Status rule-out.

However, once she was placed on the monitor her status became less clear:

Given the fast rate and possibility for SVT, atrial fibrillation, or even ventricular tachycardia the crew needed more information.

When faced with an uncertain rhythm strip it is best to acquire more leads, and a 12-Lead is a wonderful way to do so:

So what are we looking at?

Many readers pointed out the irregularly irregular tachycardia present in just about every lead.
Some readers pointed out the regular rhythm present in lead III.
Other readers noted the 3-Lead and 12-Lead were full of artifact.
Some readers gave up with cries of, "Treat the Patient! Not the Monitor!"

Ok, I can read the comments; tell me what it is!

The answer is easiest to see in the initial rhythm strip. A closer inspection reveals that when you try to line up Leads II and III, they do not even march out!

If we were to display a tracing of the pulse oximetry waveform, it would likely be more evident that only Lead III is providing a useful display.

So why did our patient's pulses not match with her cardiac rhythm?

And why did our patient have an irregular tachycardic rhythm in every lead but Lead III?

Both prehospital and hospital providers who routinely acquire electrocardiograms are familiar with artifact obscuring rhythm and 12-Lead interpretation. Common causes of artifact on the ECG include power line intereference, patient movement, and baseline wander. Lesser known causes of artifact on the ECG include cable failure, neurostimulators, lead placement over arterial pulse points, and electrode manipulation.

Cardiac monitors are designed with electrical filters which screen out intereference which is of a frequency that exists outside the range of physiologic parameters. Unfortunately, if the frequency of an artifact occurs at a near-physiologic rate it will be up to the provider interpreting the ECG to mentally "screen out" the interference.

In this case our patient has advanced Parkinson's disease, which is a degenerative neurological disorder affecting the central nervous system. The most visible symptom of this disease is the motor dysfunction and the characteristic tremors it produces in the periphery. As with any patient motion, it can cause artifact on the surface ECG.

If we take a closer look at Leads II and III we can see that the Parkinsonian Tremors present produced artifact at a rate of 250-300 and looked surprisingly like Atrial Fibrillation with WPW!

There have been multiple case reports of Parkinsonian Tremors mimicing ventricular tachycardia, ventricular fibrillation, atrial flutter, and supraventricular tachycardia. In one case, a comatose ventilated patient inappropriately received defibrillation for what appeared to be ventricular tachycardia!

When evaluating a patient with tremors it is best to place the leads in the Mason-Likar configuration, i.e. the limb leads are placed on the chest and abdomen. However, sometimes even that will not help and a switch to an anterior-posterior configuration (roughly approximating the pads position, or V4-RA and V8-LL) may be your only option to record a semi-clean tracing.

Remember, as prehospital providers it is important that we be able to explain our findings on the ECG because it may have a large impact on the patient's inhospital care.

Epilogue

Our crew was perplexed as to the discrepancy between the patient's pulse rate and that the rhythms in Leads II and III seemed, "out of sync". They contacted medical control for guidance and were advised to transport to the closest facility and to withold rate control while the patient's blood pressure was adequate.

Narcan was administered due to a persistently low SpO2 and pinpoint pupils. The remainder of the transport was unremarkable and the patient's vital signs remained relatively unchanged. A palpable pulse of 70 was weakly present at the radials while a monitored heart rate of 250-280 was given.

Upon arrival at the receiving facility the patient was noted to have converted to a normal sinus rhythm, with an RBBB and ocasional PVC's. However, during the course of her ED stay she had another "bout of tachycardia" on the monitor and was sent to the floor for observation. It is the opinion of this author that the patient's recurrent tachycardia was merely artifact, likely similar to that seen in her prehospital ECG's.

We hope you enjoyed this case as much as we did!

Posted by Christopher Watford on August 22, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, artifact, atrial fibrillation, atrial fibrillation and Wolff-Parkinson-White syndrome, case study, Christopher Watford, EMS 12-Lead, mimics, Paramedic, Parkinsonian Tremors, RBBB, right bundle branch block, wide complex tachycardia

77 year old female: Unresponsive

66 comments

This is a great case sent in my a reader who wishes to remain anonymous. We hope you find it as intriguing as we did!

After clearing up from a routine interfacility transfer, you're dispatched for a 77 year old female who is unresponsive at a local extended care facility. A BLS engine crew is enroute as well and has a few minute lead on your unit.

As you're arriving the engine crew hails you on a tac channel and relays that the patient is unresponsive, but breathing and they have put her on a NRB and are checking her blood glucose level.

You're directed to the room where the engine crew is completing their assessment of the patient. The facility staff states the patient was alert and oriented at 0600 when they did their rounds. However, when they came back at 0900 to give the patient breakfast and her morning medications they found her unresponsive.

Apparently, EMS is called frequently for this patient becoming unresponsive, although she does not know why. She hands you the patient's paperwork as the captain from the engine gives you the patient's vitals:

GCS: 8 (E2 M2 V4)
Pulse: 60, weak at the radials
BP: 118/56
RR: 16, clear bilateral lung sounds
SpO2: 82% on room air, 94% on a non-rebreather
BGL: 102 mg/dL (5.6 mmol/L)

As your partner helps the engine crew move the patient to your stretcher you read over her paperwork:

PMHx: hypertension, osteoarthritis, renal cysts, urosepsis, advanced parkinson's disease, history of UTIs, dementia, history of plueral effusion, COPD
Meds: hydrocodone, sorbitol, ferrous sulfate, dulcolak, prednisone, albuterol, ativan, heparin, aspirin, colace, sinemet, synthroid, tylenol, furosemide, potassium chloride, aricept, multi-vitamin, claritin, lactulose
Allergies: cipro, septra, florinef, bactrim, levaquin, zoloft, gentamicin

A quick physical exam reveals moaning to painful stimuli, pinpoint pupils, whole body tremors, a foley catheter with adequate output amber in color. The remainder of the exam is unremarkable.

In the back of the unit you place the patient on nasal capnography while your partner places the patient on the monitor:

At this point your partner grabs the 12-Lead cable and begins placing electrodes while you acquire an IV.

You're 10 minutes from a local hospital, and 15 minutes from a cardiac center.

What is our patient's rhythm?
What does the patient's 12-Lead show?
What are your treatment priorities?

Leave your answers below!

Looking for the conclusion? 77 year old female: Unresponsive – Discussion.

Posted by Christopher Watford on August 20, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, case study, Christopher Watford, EMS 12-Lead, narrow complex tachyardias, Paramedic

Snapshot: 64 Year Old Male–Chest Pain

31 comments

Today we have a short "Snapshot" case…Just the down and dirty.

You are called to an urgent care center for a 64 year old male, CC of substernal chest pain, which radiated to the right shoulder and neck area. He states the discomfort feels a little like "indigestion".

This episode began just after finishing a 30 minute workout on the bike.

He denies any SOB or lightheadedness, but does admit to becoming diaphoretic. However, he does not know how much of that to attribute to the workout.

Frightened, the patient drives himself to the local urgent care center .

Upon your arrival, the patient states that the discomfort had "just diminished", and that he now "doesn't feel too bad at all".

Vitals are within normal limits, and the patient does not admit to any significant history.

You acquire the following 12 lead:

What are your interpretations of this ECG? How concerned, if at all, are you?

The patient's discomfort has "diminished" by the time you arrive. How does this change affect your assessment and risk stratification of this patient?

You are 15 minutes from the local ED, and 40 minutes from a PCI center, although aviation may be available. How do you want to treat this patient?

Posted by David Baumrind on August 14, 2012 • Filed under: ems-topics, patient-management, Training • Tagged: 12-Lead ECG, case study, David Baumrind, ems12lead.com, Paramedic

Discussion for “A Change of Pace: What Happened?”

4 comments

This is the discussion for "A change of Pace: What Happened?" My apologies for the delay!

Pacemakers are amazing pieces of technology. They have evolved continually, and have given patients an increasing quality of life where none existed before.

However, with this amazing technology comes a level of complexity that also has not been seen before. These are remarkable devices, cable of many, many different types of functions. Sensing, pacing, defibrillating, single chamber, dual chamber, atrial paced, ventricular paced, cardiac resynchronization, etc… you get the idea. These are just some of the diverse functions that these devices can perform.

For us, we don't often know what type of pacemaker we are dealing with. And often, our patients do not know either! This created a dilemma for us, when we are confronted with an ill patient, and a pacemaker functioning in a way that we do not often see. Is it performing properly? Or is it performing inappropriately? Is the patient's complaint related to the pacemaker function, or the pacemaker reacting to the illness of the patient? To adequately answer these questions, we have to be able to figure our whether the pacemaker is functioning as it should, and why it is behaving this way.

To this end, I have enlisted the help of Mark Perrin, author of the EP Fellow blog. Peer sourcing is an amazing resource!

We'll go through these strips one at a time.

First, let's revisit the first ECG:

There appears to be a sinus rhythm at a rate of about 75bpm. The PR interval is about 240ms, and the QRS duration is slightly prolonged at about 110ms. There are pacing spikes that appear at the onset of the QRS. There also appears to be a fairly constant interval of 140ms between the P wave and the pacing spike.

So, what is going on here? Are the ventricles being paced by the pacemaker?

The first thing to understand is that the site of the pacing lead is normally in the right ventricle. Most of us already know that. However, what we may not all know is that the pacing lead sees "local activation", not the QRS that we see on the surface ECG.

Mark Perrin: "A pacing spike on the beginning of the QRS is not uncommon. It usually occurs because of a right bundle branch block of a right ventricular conduction delay. The pacing lead is in the RV, therefore if there is delay to the right ventricle, activation of the LV (through a conducted P through the AV node) may occur just before the RV lead paces. The RV lead paces because it has not seen LV activation."

Essentially, there is an atrial sensing window of 140ms in this case. If there is a QRS that occurs within that sensing window, the pacing spike will be inhibited. If there is no QRS impulse sensed, the pacing lead will pace. Because of the conduction delay, the beginning of the QRS (which we see) is not seen by the pacer due to the conduction delay, so it paces, even though the ventricle is already responding to the P wave. What should happen, if this occurs, is that the pacing spike should always be near the beginning of the QRS. If it is, as it is in this case, nothing needs to be done, as this is what you could call a "normal variant".

What about the pause near the end of the strip, followed by the complex that looks different from the rest? You may also notice that the P wave looks a little different as well:

Mark Perrin: "This probably occurs because of a different degree of fusion between the conducted LV activation and RV pacing. The change in the apparent AV interval occurs again because the atrial lead sees "local" activation, not the P wave on the surface ECG. Therefore if the atrial activation occurs closer to the AV node it may start conducting to the ventricle before the wavefront reaches the atrial sensing bipole and triggers ventricular pacing. The opposite also occurs, i.e. atrial activation is further from the node, and reaches the atrial sensing bipole long before getting to the AV node."

Let's take a look at the second strip again:

This strip is a variation on the theme of the first. This strip has a mixture of the complexes seen on the first ECG, some with varying degrees of fusion, plus a fully paced beat near the end of the strip. Why the fully paced beat here?

Mark Perrin: "The fully paced beat occurs (my guess) because the PVC before it invades the AV node thus delaying conduction down the node on the following beat."

Now on to the third ECG:

Here we see a fully paced rhythm at a rate of about 85bpm. Why the change from the prior rhythm to a fully paced rhythm?

To fully understand this, we have to remember a bit of physiology. In older people, or others likely to have diseased conduction systems, the "native" AV interval often increases when the heart rate increases. As the sinus rate increases, as in this case, the native AV interval also increases to the point where it is now longer than the pacemaker AV interval. Anytime the pacemaker AV interval is shorter than the native AV interval we won't see normal conduction anymore as the pacemaker takes over.

For this patient, these strips show normal pacemaker behavior. The main concept to remember is that the pacemaker does not see what wee see on the surface ECG. The pacemaker see local activation which may occur after the onset of the QRS in the ventricles, or after the onset of the P in the atria.

Many thanks again to Mark Perrin. I hope you have learned as much as I have in this case. I find pacemaker rhythms to be challenging but rewarding. They can behave in so many different ways..Normally sometimes, and abnormally others. They really are incredible pieces of technology, and I one day aspire to really master the many ways in which they work. One day!

Posted by David Baumrind on August 3, 2012 • Filed under: command-leadership, Dispatch & Communications, ems-health-safety, ems-topics, mass-casualty-incident, patient-management, technology-communications-ems-topics, Training, training-development, training-fire-rescue-topics • Tagged: AICD, case study, David Baumrind, ems12lead.com, pacemaker

Stump the Chumps: Atropine and Complete Heart Block – Discussion

6 comments

This is the conclusion to our special feature Stump the Chumps: Atropine and Complete Heart Block. If you've not seen the case, I recommend you go back and read it over.

To recap, our crew had been dispatched to a 63 year old female who was lightheaded and happened to have a bit of a bradyarrhythmia.

Ok, she had a lot of bradyarrhythmia.

Let's review that first 12-Lead ECG:

We've got a wide complex, regular ventricular rhythm at a rate of 30. A regular atrial rhythm is present as well at a rate of 140. What is most interesting in this case is the degree of AV nodal conduction present. The PRi appears fixed at 0.16s for most of the strip, however, the first complex has a much shorter PRi.

After the administration of atropine, while prepping for transcutaneous pacing, we had two rhythm changes:

Reviewing the subsequent 12-Leads shows a progression to 2:1 AV Block, then 1:1 conduction and sinus tachycardia.

Here at EMS 12-Lead, we had come up with two competing theories for the first 12-Lead:

Complete heart block
2nd Degree AV Nodal block Type II, 4:1 conduction

In favor of a complete heart block is a wide complex rhythm with morphology suggesting a left ventricular escape, large bizarre T-waves, inconsistent PR interval, and a change in morphology after the change to a 2:1 AV Nodal block.

In favor of a 4:1 heart block is the apparent fixed PR interval between all three ECG's, with a progression from 4:1 to 1:1 conduction after the administration of atropine.

This is a tough case!

The team here at EMS 12-Lead couldn't come to a definitive answer for you folks, so we branched out. Part of what makes EMS 2.0 great are the doctors who have made themselves available to answer these tough questions. In fact, Drs. Ken Grauer and Arnel C. provided their expert rhythm analysis on this case!

Shortly after we received it, I sent this case over to Dr. Mark Perrin (@EPFellow), an electrophysiologist fellow, to get his take. What was the rhythm? Why did it appear to change with atropine? Well, he had this to say:

These are interesting ECGs. I think the different manifestations are all explained by the sinus rate:

ECG '0' at 9:50 pm – is sinus cycle length 470 ms (Ed: sinus cycle length is the P-P interval), CHB (PR differs on the first two beats, and the complex is more consistent with a ventricular focus, note the reversal of 'rabbit ears' in V1 – sometimes used to differentiate SVT from VT).

ECG '1' 10:18 pm – sinus CL 520 ms, now 2:1 AV block and showing the morphology of conducted beats which is very different from the first ECG.

ECG '2' 10:20 pm – sinus CL 580 ms. Now 1:1 conduction, with conduction disease LAFB, and RV delay/RBBB as in ecg '1'.

So I think this is an example of acceleration dependent CHB.

In a tachycardia dependent complete heart block, the AV node fails to conduct often after the atrial rate increases beyond a critical rate. As the sinus rate in our patient slowed, the degree of AV block improved!

So, how did atropine help this patient? Dr. Perrin continued:

My interpretation is sick/sob for other reasons initially, increased sinus rate -> CHB, felt even more terrible and afraid, sinus rate increases further….friendly paramedic arrives, reassures, sinus rate slows, and conduction returns. I think the atropine did nothing. This is an example of why atropine can actually make this kind of heart block worse, It tends to increase sinus rate, and a high sinus rate can increase the severity of heart block. But the most common effect of atropine is to do nothing…as is probably the case here (unless you posit it somehow reducing the sinus rate) – the level of block is below the AV node.

Many of our readers acknowledged this to be the likely reason for our patient's improvement. In the hospital this patient should receive a permanent pacemaker. Unfortunately the patient was lost to follow-up to the EMS crew.

So there we go, positioning, fluid, and some tender love and care can go a long way in some patients!

Posted by Christopher Watford on July 12, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, atrioventricular blocks, AV Block, bradycardia, case study, Christopher Watford, complete heart block, EMS 12-Lead, Paramedic, unstable bradycardia

Stump the Chumps – Atropine and Complete Heart Block

18 comments

This great case was sent in by an anonymous reader posed as a question, the likes of which we had not seen before. So, to pay homage to a wonderful radio show signing off this year, we're calling this segment: Stump the Chumps!

Our reader was dispatched to back up a crew attending to a 63 year old female complaining of lightheadedness.

The original crew had found her to be confused, lethargic, with nearly absent radial pulses, and pale clammy skin. The patient denies chest pain and shortness of breath, and adamantly denies any cardiac history. Only history of note is a recent trip to Southeast Asia over a month ago.

Her vitals were as follows:

Pulse: 30 bpm, palpable at the brachial
BP: 80 mmHg systolic, unable to auscultate a diastolic (LP12 unable to acquire as well)
RR: 14, lung sounds clear and equal
SpO2: 98% r/a
BGL: 124 mg/dL (6.9 mmol/L)

The patient was hooked up to the cardiac monitor and a 12-Lead ECG was obtained. During acquisition of this 12-Lead, the crew established intravenous access.

After acquisition, it was decided to begin transcutaneous pacing. While the procedure was explained to the patient, 0.5 mg of atropine was administered via IV and combo-pads were placed.

A few minutes after the administration of atropine, the crew noticed a change in the rhythm and acquired a second 12-Lead.

The patient's blood pressure and skin color improved.

A few more minutes pass and again a rhythm change is noted on the monitor. Another 12-lead is acquired.

At this point, the patient has improved significantly and transcutaneous pacing is no longer necessary. The remainder of the transport was uneventful and in the hospital the patient was recommended for permanent pacemaker insertion.

We're left with a number of questions:

Is the first 12-Lead a complete heart block? And if so, why did atropine work?
What does the second 12-Lead show?
What does the third 12-Lead show?

So, before we attempt to answer these questions, we'd like to hear what you think!

Posted by Christopher Watford on July 3, 2012 • Filed under: ems-topics, patient-management • Tagged: 12-Lead ECG, atropine, bradycardia, case study, Christopher Watford, Paramedic, Stump the Chumps, transcutaneous pacing, unstable bradycardia

65 year old male CC: Fall with injury – Conclusion

10 comments

This is the conclusion to 65 year old male CC: Fall with injury. You may wish to review the history and clinical presentation.

When we left off the patient was in severe heart failure with the following 12-lead ECG.

As we have mentioned before on several occasions, the most important thing when treating a patient with a tachycardia is to decide whether or not the tachycardia is causing the symptoms or the symptoms are causing the tachycardia.

In other words, you should try to rule out the possibility that it's a compensatory tachycardia. As this case clearly demonstrates, this can be very difficult!

The crew felt that the differential diagnosis for this wide complex tachycardia (from most likely to least likely) was VT, 2:1 atrial flutter with LBBB, sinus tachycardia with LBBB, or some other SVT with aberrancy.

Due to the patient's instability, the treating paramedic felt there was little to lose and much to gain by attempting synchronized cardioversion. If the rhythm was VT or 2:1 flutter the patient's condition might improve dramatically. If it turned out to be sinus tachycardia with LBBB he'd be in the exact same position.

Attempt #1

Attempt #2

There appeared to be no change in the heart rhythm.

A report was given to online medical control and the patient was transported emergently to the hospital.

On arrival the patient was placed on BiPAP and started on a NTG drip.

Here was the 12-lead ECG on arrival.

The patient was given lopressor 5 mg slow IV push.

The conversion rhythm shows sinus rhythm at 92 bpm with left bundle branch block.

So, we now know that the patient probably had LBBB at baseline. However, without a heart rate histogram it's difficult to say whether or not this was 2:1 flutter that converted sinus rhythm or sinus tachycardia that was slowed down with the lopressor.

This is often overlooked in the emergency setting but in the inhospital setting it's very important to document the onset or termination of an arrhythmia for this very reason.

The patient's SpO2 came up above 90% and the patient became more alert and was attempting to communicate by the time EMS was done writing their report. No further information is available.

Posted by Tom Bouthillet on July 2, 2012 • Filed under: ems-topics, patient-management • Tagged: case study, ECG, EKG, EMS, EMS 12-Lead, ems12lead.com, left bundle branch block, Paramedic, Prehospital 12-Lead ECG blog, VT versus SVT with aberrancy, wide complex tachycardia

65 year old male CC: Fall with injury

57 comments

Here's a very interesting case submitted by a faithful reader who wishes to remain anonymous. Some changes have been made to preserve patient confidentiality.

EMS is called to a local breakfast restaurant for a 65 year old male who fell in the parking lot. He was reported to have suffered a head injury.

On arrival the patient is found sitting in his car. He appears critically ill. Skin is pale and diaphoretic. Nail beds are blue. The patient's level of consciousness is significantly diminished. His shirt and pants are wet and it's not clear if he was incontinent of urine or spilled a drink on himself. He has audible expiratory rales without the need for a stethescope.

The patient states that he tripped and fell. His wife states that he was "fine" prior to falling but she does not impress EMS as a good historian. When asked about his history she says, "heart."

The head appears atraumatic with the exception of some abrasions to the face. He admits to head pain "all over" and keeps muttering "please take me to the hospital."

Due to the patient's diminished level of consciousness it is not possible to clear the cervical spine with any established criteria. However, the paramedics conclude that the patient cannot be laid flat and elect to defer spinal immobilization. The patient is placed on the gurney with the head elevated and vital signs are assessed.

RR: 30
HR: 148
NIBP: 150/77
SpO2: 58 on room air

The patient is placed on a NRB mask @ 15 LPM. The chest is exposed and no chest trauma is apparent. Breath sounds: rhonchi and rales bilaterally

The patient is given a dose of SL NTG and loaded in the back of the ambulance. At this point the patient appears peri-arrest.

The cardiac monitor is attached.

A 12-lead ECG is obtained.

What would you do next?

51 Year Old Male: Chest Pain

20 comments

Here is a great case submitted by faithful reader Niels, a Paramedic in Germany. As always, some minor information may have been changed to preserve patient confidentiality.

Our case today takes us overseas, to the German countryside. It's a clear blue Monday morning, 11:40 am, when you and your partner are called to a 51 year old male complaining of chest pain. You are dispatched parallel to an Emergency Physician (in Germany, every ALS call is dispatched with an ALS ambulance and a doctor).

On arrival, you find a male patient lying in bed. He appears to be very diaphoretic an pale. He tells you he is very athletic and fit, but today is "feeling horrible". He says his "chest is killing him", and he admits to being nauseous, with several bouts of vomiting.

O,P,Q,R,S,T: He tells you he woke up with the pain, and it seemingly came out of the blue–he was feeling fine the night before. Nothing seems to make the pain, which he describes as "crushing', feel better. In fact he can find no position of comfort. You seem to be compiling "red flags" as he tells you that the substernal pain also radiates to his left arm. He rates it a 4 or 5 out of 10, and says it began about 15 minutes before EMS was called. You ask if he's ever had this happen before and he says no.

As your partner starts to apply the electrodes, you continue your HPI and vitals. He has no real medical history, although he did smoke but quit ten years ago. He takes no meds. He does tell you that he saw his general physician last week for becoming "short of breath" during his workouts. Pneumonia was ruled out.

HR: 67 and regular
BP: 92/57
RR: 28, a bit labored
Skin: cool and moist
Lungs Clear, SpO2 99% on room air

You give him 4 baby ASA, and acquire the following 12 lead ECG:

Ok, this is not what you are used to seeing. In addition, the speed is 50mm/sec. Thanks to the studio magic of Christopher Watford, here is the same ECG "stitched" together in the familiar format, speed adjusted to 25mm/sec:

A few moments later, the Physician arrives. He wants to know the status of the patient, and what you see on the ECG.

What do you tell him?

Posted by David Baumrind on June 20, 2012 • Filed under: ems-health-safety, patient-management, Training, training-development • Tagged: 12-Lead ECG, case study, Chest Pain, David Baumrind, ems12lead.com, Paramedic

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