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47 year old male: Holiday Indigestion – Conclusion

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

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

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

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

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

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

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

ST-depression from ischemia does not localize.

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

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

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

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

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

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

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

Frightful Weather We're Having - Cath Pictures

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

  • Sometimes STEMI patients will have atypical symptoms.
  • A single ECG is not enough to detect all STEMI patients, serial 12-Lead ECG's should be acquired on all patients who receive one.
  • ST-depression from ischemia does not localize, localized ST-depression should be considered a reciprocal change until proven otherwise.

47 year old male: Holiday Indigestion

18 comments

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

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

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

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

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

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

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

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

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

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

Frightful Weather We're Having - Initial 12-Lead

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

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

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

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

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

  • What do these 12-Lead's show?
  • What are your next steps?
  • Is indigestion a contraindication to aspirin administration?
  • Are you glad this case does not involve a narrow complex tachycardia?

63 year old male CC: Substernal Chest Pain

15 comments

Today we're presenting a case from our friend Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. In fact, this case is being presented both for his readers and for ours! We hope you like it.

You're working ED triage when a 63-year-old man walks in complaining of substernal chest pressure that had awoken him from sleep 2 hours prior. He denied any radiation of the pain, but complained of some mild presyncopal symptoms. His wife reported that he had had intense diaphoresis at home. He reported having a similar episode 1 year ago, but a subsequent stress test was negative. 

You obtain a quick history:

  • PMHx: HTN, type 2 diabetes mellitus
  • Meds: irbesartan, insulin
  • Allergies: NKDA 

A quick set of vitals are obtained:

  • HR: 90 
  • BP: 145/123 (NIBP)
  • RR: 16, unlabored
  • SaO2: 98% r/a

The physical exam reveals a patient with mild sweating, but no JVD. His lungs are clear, there are no cardiac murmurs, and he does not have any lower extremity swelling or tenderness.

You obtain a STAT 12-Lead ECG:

I Think Your Segments are Upside Down - Initial 12-Lead

The patient is taken back to a bed, 324mg of aspirin is administered, an IV is started, and labs are drawn. The patient receives 0.4 mg SL nitroglycerin and 5 mg morphine, both without relief. Metoprolol is given for the patient's hypertension and a heparin drip initiated. Cardiology was consulted and believed the ECG to be non-specific. 

Per the ED physician, an ECG is performed 15 minutes later to assess the right side of the heart. Note that all of the precordial leads were reversed (e.g. V2R = V1):

I Think Your Segments are Upside Down - Right-Sided 12-Lead

Due to persistent chest pain, a nitroglycerin drip is initiated and titrated up to 132 mcg/min without improvement in chest pain. A loading dose of clopidogrel is given.

An hour after presentation the ED physician asks for a posterior ECG:

I Think Your Segments are Upside Down - Posterior 12-Lead

Labs return a troponin of 0.05 (normal is < 0.04). A CBC and basic chemistry panel were essentially negative.

 

  • What does the first ECG show? Is it diagnostic?
  • Do the right-side and posterior leads help with diagnosis? 
  • If this is a STEMI, what coronary artery is likely involved? 

24 year old male: “Anxiety Attack” – Conclusion

11 comments

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!

Happens All the Time Man - Initial Rhythm Strip

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.

Happens All the Time Man - Initial 12-Lead

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:

Happens All the Time Man - Vagal Attempt

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:

Happens All the Time Man - Adenosine

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:

Happens All the Time Man - Post-conversion 12-Lead

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?

62 year old male: Chest Discomfort – Conclusion

1 comment

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.

Well Page Him Again - Initial 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:

Well Page Him Again - Repeat 12-Lead

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 ***.

Well Page Him Again - Wellens Syndrome

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]

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:

Happens All the Time Man - Initial Rhythm Strip

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:

Happens All the Time Man - Initial 12-Lead

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

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:

Well Page Him Again - Initial 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?

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:

Round and Round He Goes - Initial Rhythm

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.

Round and Round He Goes - Initial 12-Lead

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.

Round and Round He Goes - 6mg Adenosine Bolus

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.

Round and Round He Goes - After first Adenosine

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.

Round and Round He Goes - 12mg Adenosine Bolus

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

Round and Round He Goes - After second Adenosine

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.

Round and Round He Goes - After 10mg Cardizem Bolus

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.

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.

Round and Round He Goes - Initial Rhythm

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

Round and Round He Goes - Initial 12-Lead

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?

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.

All Over the Map - Rhythm Strip

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

All Over the Map - 12-Lead

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:

Lewis Lead Placement

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:

All Over the Map - Lewis Lead - Marked Up

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!

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:

We'll See What Shakes Out - Rhythm Strip

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:

We'll See What Shakes Out - 12-Lead

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!

We'll See What Shakes Out - Rhythm Strip Marked Up

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!

We'll See What Shakes Out - Lead II and Lead III

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!

77 year old female: Unresponsive

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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:

  • PMHxhypertension, osteoarthritis, renal cysts, urosepsis, advanced parkinson's disease, history of UTIs, dementia, history of plueral effusion, COPD
  • Medshydrocodone, sorbitol, ferrous sulfate, dulcolak, prednisone, albuterol, ativan, heparin, aspirin, colace, sinemet, synthroid, tylenol, furosemide, potassium chloride, aricept, multi-vitamin, claritin, lactulose
  • Allergiescipro, 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:

We'll See What Shakes Out - Rhythm Strip

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

We'll See What Shakes Out - 12-Lead

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.

Stump the Chumps: Atropine and Complete Heart Block – Discussion

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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:

Stump the Chumps - Initial 12-Lead

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:

Stump the Chumps - Post Atropine 1

Stump the Chumps - Post Atropine 2

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!

65 year old male CC: Fall with injury – Conclusion

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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.

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?

See also:

65 year old male CC: Fall with injury – Conclusion

56 year old female CC: Short of Breath – Conclusion

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This is the conclusion to 56 year old female CC: Short of Breath. Be sure to check out the first post for the full story!

When we left our crew they were just getting ready to leave the parking garage with a 56 year old female who was short of breath and dizzy after mild exertion. They had obtained IV access, a 3-Lead, and a 12-Lead ECG.

Let's review our patient's 3-Lead:

Breathless View - Initial Rhythm

This is a regular, narrow complex tachycardia at 120 bpm with what appear to be sinus P-waves best appreciated in leads II and aVF. Given our patient's tachypnea and dizziness, her tachycardia is likely a compensatory mechanism.

It is important that we find out what her body is compensating for!

Perhaps her 12-Lead can clue us in on her malady?

Breathless View - 12-Lead

Her 12-Lead shows a sinus tachycardia with an incomplete right bundle branch block (the QRS duration is 100ms) and some diffuse ST/T-wave changes including some T-wave inversion and ST-depression.

These changes, when taken in the context of our patient's breathlessness strongly suggest the patient is suffering from a pulmonary embolism! Given her chest pain, we should also consider acute coronary syndrome as her problems as well.

However, as Dr. Smith notes, T-wave inversions in Lead III and the anterior precordials are far more common in PE than in acute coronary syndrome.

I've marked up the 12-Lead to highlight some of the key features, including the S1Q3T3 pattern, incomplete right bundle branch block, and anterior T-wave inversions:

Breathless View - 12-Lead - Marked Up

The patient's condition remained stable throughout the transport and the crew elected to continue oxygen therapy and administer a fluid bolus.

While the surface ECG is not sensitive nor specific for pulmonary embolism, it often times can provide clues as to the diagnosis. Here is a list of changes seen in Pulmonary Embolism on the ECG adapted from Chou's Electrocardiography in Clinical Practice ordered by their prevalence:

  1. Sinus tachycardia (73%)
  2. Prominent S-wave in Lead I (73%)
  3. "Clockwise rotation" / late precordial transition (56%)
  4. T-wave inversion in 2+ precordials (50%)
  5. Incomplete or complete RBBB (20-68%)
  6. P-pulmonale (28-33%)
  7. Right axis deviation (23-30%)
  8. No significant findings (20-24%)
  9. S1Q3T3 (12-25%)
  10. Supraventricular arrhythmias (12%)

During her stay in the emergency department it was confirmed that she was experiencing multiple small pulmonary emboli, and given their size they elected to start her on low molecular weight heparin and observe the patient overnight.

56 year old female CC: Short of Breath

21 comments

Many thanks to an anonymous reader who submitted this great case! As always, some details have been changed to protect provider and patient privacy.

You're dispatched to the parking garage of a busy shopping mall for a 56 year old female whom a 3rd party caller relates is, "short of breath".

Upon your arrival you find an engine crew out with the patient, who is seated on the running board under the pump panel on their engine. The firefighters have placed her on a nasal cannula and are attempting to talk with her through a bystander.

The captain on the engine relays that she doesn't speak much English, but what they gather is that she was walking back to her car and became short of breath and dizzy. The patient states she felt better sitting and on oxygen.

Your partner relays the first set of vitals:

  • Pulse: 130, regular
  • BP: 132/80
  • RR: 28
  • SpO2: 89% on r/a, increasing to 94% @ 4 L/min by NC
  • Lungs: clear and equal bilaterally

The bystander helps translate her history:

  • Allergies: None
  • Medications: None
  • PMHx: None
  • Last ins/outs: Some urinary incontinence handled through PO restriction
  • Events: Walking to her car, became short of breath and dizzy, denies loss of consciousness, she is visiting from another country and was on a "long flight" last week

You ask if the patient would like to go to the hospital and she nods her head. When the crew stands her up to help her to your stretcher, she becomes dizzy and clutches her chest. Once on the stretcher your partner places her in trendelenburg as you move her to the unit.

Inside, your partner places her on the monitor while you complete a physical assessment. Her skin color appears fine, but you notice some pedal edema. Old scars are present on her knees which the patient states was from surgery. She denies pain to palpation of her chest wall and her lung sounds remain clear bilaterally. Her physical exam appears largely unremarkable.

Her radial pulse is a bit weaker and has slowed to 120 bpm. She remains tachypneic, but denies chest pain once she was laid down. Her SpO2 has increased to 97% on 4 L/min and her respiratory rate has decreased slightly.

Breathless View - Initial Rhythm

As you start an IV, your partner acquires a 12-Lead.

Breathless View - 12-Lead

Your partner asks if you need anything else before you head enroute to the hospital.

  • What is the patient's rhythm? What does the patient's 12-Lead show?
  • Does this patient require any interventions before going to the hospital?
  • What type of hospital does this patient need?
  • What do you think is wrong with this patient?

Comparing 12-Leads: Discussion

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This is the discussion for Comparing 12-Leads: Common Error or Common Disease? All of our readers were on the right track, and many were spot on!

Sometimes, troubleshooting an ECG is more than just lead placement. In this case report, we had three 12-Lead ECG's, all featuring a similar pattern: inappropriate R-wave progression.

You Take the Lead - Inappropriate R-wave Progression

Initially, when reviewing the first of these ECG's, I had believed it to be lead placement error. The most likely cause of inappropriate R-wave progression and low voltage in a precordial lead is the placement of the electrode on the mammary tissue or on the abdomen.

After reviewing two more ECG's from two different shifts, it became evident that the problem was more likely with the equipment than operator.

Two of the paramedics on duty were alerted to the possibility of a malfunctioning cardiac monitor, and the same was taken out of service for testing. During their investigation, it was found that the cables themselves were at fault.

The following is a 12-lead ECG acquired from one of the Paramedics using the current set of malfunctioning LP15 cables:

You Take the Lead - 12-Lead Comparison: Bad Cables

A set of LP12 cables was then connected to the same Paramedic and then connected to the same cardiac monitor:

You Take the Lead - 12-Lead Comparison: Good Cables

The difference in these 12-Lead ECG's is striking.

Remember, R-waves should progress in a continuous fashion from V1 through V6. Usually with a transition from negative to positive around leads V3 and V4. This is known as good R-wave progression.

R-Wave Progression - The Textbook of Medical Physiology 9e; © 1996 Guyton AC, Hall JE; WB Saunders.

With Paced Rhythms, RBBB, LBBB, RVH, LVH, or myocardial infarctions this zone of transition and R-wave progression may be early or delayed. You'll often hear about poor R-wave progression or an early or late transition. These refer to the change in dominant polarity across the precordial leads, whether from positive to negative or vice versa.

In any case, the changes must be continuous. Any discontinuity indicates a problem in acquisition.

Whenever you review a 12-Lead, be sure to consider the validity of the tracing beyond simple interpretation. You should be checking for baseline wander, excessive artifact, and electrode placement.

  • What types of machine failures have you seen that have gone unnoticed?
  • Do you have a QA program in place to assess the quality and accuracy of 12-Lead ECG acquisition?
  • Does your department discuss data quality issues during training?

See also:

Precordial Leads – The Transition, R-Wave Progression, R/S Ratio in Lead V1

69 year old female CC: Shortness of breath, weakness

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Here's a case submitted by a faithful reader who wishes to remain anonymous. He has submitted several cases before and they are always excellent so thank you, Mr. Anonymous! 

EMS is called to the residence of a 69 year old female who is complaining of sudden onset of shortness of breath and weakness.

  • Past medical history: Healthy
  • Medications: None

The patient is seen in the emergency department of a local community hospital where she is found to have slight J-point elevation in the anterior leads.

(The vital signs and results of the physical exam are not available.)

Approximately 2 hours later there is a slight change in ST-segment morphology and new T-wave inversion in lead aVL. A cardiologist is consulted via telemedicine at the tertiary care center and the decision is made to transfer the patient.

Concurrently with this decision the patient is given 3 doses of SL NTG with complete resolution of her symptoms.

The transport ambulance arrives and records the following 12-lead ECG.

Several more are recorded en route. Here's the ECG captured on arrival at the PCI-hospital.

Do you think this patient is having a STEMI? Why or why not?

88 year old male CC: Chest pain

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EMS is called to a 88 year old male with a chief complaint of chest discomfort.

On arrival the patient meets EMS at the front door. His skin is slightly pale and moist. He appears anxious.

  • Past medical history: "Cardiac", pacemaker, hypertension, dyslipidemia
  • Medications: Numerous, unavailable at the time of EMS evaluation

Paramedics lead the man to a chair and the assessment begins.

  • Onset: 30 minutes prior to EMS arrival
  • Provoke: Nothing makes the pain better or worse
  • Quality: Poorly localized pressure
  • Radiate: Does not radiate
  • Severity: 7/10
  • Time: Admits to previous episodes but unable to give details

Vital signs are assessed.

  • RR: 18
  • Pulse: 70
  • NIBP: 140/92
  • SpO2: 90 on RA

Breath sounds: Clear in the apexes, diminished in the bases.

No JVD or pitting edema.

The patient is placed on the cardiac monitor.

A 12-lead ECG is obtained.

The patient is placed on oxygen via NC @ 4 LPM and is removed to the back of the ambulance. An IV is initiated and the patient is given 0.4 mg NTG spray SL.

The pain subsides to 3/10.

En route an additional 12-lead ECGs is obtained.

And one more just prior to arrival.

Do you see anything here to be concerned about?

See also:

88 year old male CC: Chest pain – Conclusion

64 year old female CC: Trouble Breathing

46 comments

Thanks go to Michael Herbert for this great case! As always, some details have been changed to protect patient privacy.

It's late into your shift when the tones go off for breathing problems at a local extended care facility. Enroute you're advised it is a 64 year old female with a "low O2 sat," and to, "use the main entrance."

As you arrive a staff member is waiting for you at the door and directs you to a familiar room. The patient, a larger woman well known to your unit, is noticably anxious and struggling to breathe even on a nasal cannula.

The staff informs you she's not been feeling well all day, and only recently developed shortness of breath. Your partner places the patient on a non-rebreather at 15 L/min and grabs a quick set of vitals.

A quick look at the patient reveales pale skin, circumoral cyanosis, pink frothy sputum, and a respiratory rate in excess of 30. She has a long cardiac history, and is often transported by your service. Your partner relays her vitals:

  • Pulse: 120 bpm, weak radials
  • B/P: 110/74
  • SaO2: 78% on 2 L/min via NC
  • Resps: 36, shallow
  • BGL: 224 mg/dL

Auscultation of her lungs reveals rales in all fields.

Your partner asks if you'd like to put her on the monitor and you reply, "let's get moving and get it in the truck."

Once in the back of the truck you begin attaching the monitor, while your partner prepares CPAP. Her oxygen saturations have improved to 89% and her pulse and respirations have decreased noticably on the non-rebreather.

The rhythm strip is obscured due to patient movement, however, the 12-Lead prints out without issue.

You're 20 minutes from a PCI capable center and 5 minutes from a community hospital where the patient's physician often has her transported.

What does this 12-Lead ECG show?

What interventions does this patient need?

Do you need anymore information to make the appropriate treatment and transport decision?

18 year old male: Structure Fire Rehab – Conclusion

2 comments

Apologies for the delay, your author has been working nights and on the road traveling! We now return you to your regularly scheduled program.

This is the conclusion to 18 year old male: Structure Fire Rehab.

On the Attack Line - (c) 2011 Michael Herbert

When we left off, we had a young firefighter in our rehab area with an elevated heart rate and positive orthostatics.

He admitted to consuming energy drinks and not hydrating well, however, he had no real complaints. A 3-Lead and 12-Lead were acquired.

A look at the initial 3-Lead shows a heart rate of around 190, with P-waves buried in the preceding T-waves. The notes from the rehab officer indicate this was acquired while the patient was standing. The differentials for this rhythm include sinus tachycardia and SVT. However, given the patient's age and recent activity sinus tachycardia is the more likely diagnosis.

The 12-Lead acquired confirms our suspicions, as once the patient was sat down the rate decreased and the P-waves became more  obvious. This is sinus tachycardia with rate related ST/T-wave changes. There is no apparent ischemia or injury present. Some readers noted the rSR' in V1 and V2, however, these are most likely due to lead positioning (one intercostal space too high).

After 15 minutes of rehab he's had a water and a sports drink, with some improvement in his vital signs and no real complaints. However, they are not what we would like!

  • Pulse: 160, regular at the radials; 180 when standing
  • BP: 112/74
  • Resps: 20, unlabored
  • SpO2: 94% r/a
  • SpCO: 0%

The rehab officer was then asked by a line officer if the young firefighter could return to duty.

The most important consideration is our general impression of the patient and our findings from our physical assessment. In this case the rehab officer felt the patient had overexerted himself, was dehydrated, and was not fit for duty.

Instead, the rehab officer had the patient continue with oral intake of water and sports drinks (alternating), and reassessed the patient at regular intervals. After 30 minutes in rehab the following 3-Lead was obtained:

Put Me In Coach! - Final 3L

This is an uncomplicated sinus tachycardia. The patient's vitals were as follows:

  • Pulse: 100, regular at the radials; unchanged when standing
  • BP: 118/80
  • Resps: 16, unlabored
  • SpO2: 98% r/a
  • SpCO: 0%

At this point the fire was well under control and overhaul was in progress. The rehab officer did not allow the firefighter to return to duty, instead recommending he be transported for evaluation. The firefighter adamantly denied compaints and ultimately refused transport. He was educated on the importance of rehydration and the detrimental effects of sodas and energy drinks during exertion.

In this case IV fluids were withheld in favor of PO fluid replacement. Policies for rehydration may differ by department, however, if the patient is able to drink PO fluids, these should be preferred over IV supplement. Many marathons and triathlons have begun favoring PO over IV rehydration as well.

This course of treatment may surprise many of our readers, however, there is no data to support favoring IV fluids over PO fluids in a patient with hemodynamic changes secondary to exertion. IV fluids should instead be considered when there is symtomatic cardiovascular instability or the patient cannot effectively rehydrate orally1,2.

If your department is involved in the rehab of firefighters, you should have an NFPA 1584 compliant policy3,4 in-place with appropriate rehydration protocols.

A 24 hour call-back found the firefighter in good health and without complaint.

  1. Casa DJ, et al. Intravenous versus oral rehydration during a brief period: responses to subsequent exercise in the heat. Med Sci Sports Exerc. 2000; 32(1):124-33. [PubMed]
  2. van Rosendal SP, et al. Intravenous versus oral rehydration in athletes. Sports Med. 2010; 40(4):327-46. [PubMed]
  3. National Fire Protection Association (NFPA) 1584, Standard on the Rehabilitation Process for Members during Emergency Operations and Training Exercises. Quincy, Mass: NFPA, 2008. [Overview]
  4. McEvoy M. The Elephan on the Fireground: Secrets of NFPA 1584-Compliant Rehab. Fire Engineering. Aug 2008; 161(8). [Full Text]

90 year old male CC: “Possible stroke” – Conclusion

1 comment

This is the conclusion to 90 year old male CC: "Possible stroke". You might want to go back and familiarize yourself with the details of the case. Let's take another look at the 12-lead ECG.

Now with the computerized interpretive algorithm.

On Facebook I had asked whether or not this ECG showed signs of ischemia.

This ECG shows ST-depression in the lateral leads (I, aVL, V5 and V6) and modest ST-elevation in the right precordial leads (V1-V3). That's because it shows a strain pattern or secondary repolarization abormality due to left ventricular hypertrophy.

According to at least one study this is the most common cause of ST-elevation in chest pain patients. Hence, it is a very important pattern for paramedics to recognize in the field (although it's rare for LVH with strain to fool the GE-Marquette 12SL interpretive algorithm).

How would we know it's a strain pattern?

When we look at any 12-lead ECG we should consider the Six Step Method (or some other standardized approach).

Here we see that the patient is in sinus rhythm with a normal frontal plane axis. The QRS duration is < 120 ms so it's not a bundle branch block or paced rhythm.

At this point we might pick up on ST-depression in the lateral leads but it's too early to call it ischemia. We need to consider other possible causes. Since left ventricular hypertrophy often presents with ST-depression in the lateral leads that is a likely culprit.

Let's add the depth of the S-wave in lead V2 with the height of the R-wave in lead V5 (or V6 — they're both about the same). Is the result equal or greater than 35 mm?

Yes!

You don't need calipers for this because it doesn't have to be perfect. 35 mm is 7 large blocks so eye-ball it. The S-wave in lead V2 is at least 4 large blocks deep (it's actually more than 5 but this is the "fast and dirty" method) and the R-wave in lead V6 is at least 3 large blocks in amplitude. That's greater than 35 mm so you've met the criteria.

There are other criteria for LVH but this is the most important for ruling out STEMI mimics because LVH is usually an anterior STEMI mimic so the most important issue here is the depth of the S-waves in the right precordial leads (V1-V3). With a "strain pattern" the deeper the S-waves the more pronounced the secondary ST-T abnormality in the opposite direction.

Conversely, the taller the R-waves, the more pronounced the ST-depression and T-wave inversion. A lot of people talk about the shape of the ST-segments and T-waves in the presence of LVH, how it should be asymmetrical and upwardly or downwardly concave. That's ususally true but it's not always the case.

In this case the "strain pattern" is fairly modest. The ST-elevation in V1-V3 is not particularly impressive. Other times the result can be quite profound.

If you're still not clear on what a "strain pattern" is with LVH, take a look at the precordial leads. The QRS complex starts out negative in lead V1 and ends up positive in lead V6. The transition lead is lead V4 (which is equiphastic). As the QRS complex transitions from negative to positive, the T-wave transitions from positive to negative.

That's what we call a "widened QRS/T angle" which means that there is more than 100 degrees difference between the QRS axis and the T-wave axis. Let's take a look at the computerized measurements. The QRS axis is 16 degrees and the T-wave axis is 148 degrees.

To be much simpler about it, with a strain pattern positive QRS complexes have negative T-waves and negative QRS complexes have upright T-waves. (You should not include isoelectric or equiphasic QRS complexes in this analysis).

The general appearance of this 12-lead ECG is one of T-wave discordance. That's a finding that should almost always make you pause and consider that you're dealing with a secondary ST-T abnormality — in other words a STEMI mimic.

This patient received a fairly extensive workup for his near-syncope including a CT scan and nothing was found. He was discharged from the emergency department.

You can find previous posts about left ventricular hypertrophy here.

See also:

The Code STEMI Web Series comes to First Responders Network! 

90 year old male CC: “Possible stroke”

32 comments

EMS responds to a 90 year old male with a "possible stroke".

On arrival the patient is found sitting on the toilet (lid down). His spouse states that he had walked outside to retrieve the newpaper when he lost his balance and skinned his knee. She helped him inside and sat him down on the toilet in the bathroom when his eyes rolled back in his head and he started "shaking all over".

At the time of evaluation he is conscious, alert and oriented to person, place and time. He remembers falling while retrieving the newspaper but denies losing consciousness in the bathroom.

His skin is pale and diaphoretic.

He denies chest pain or shortness of breath.

Past medical history: Mild cognitive impairment, HTN, dyslipidemia

Medications: Metropolol, donepezil (Aricept), lovastatin (Mevacor)

Vital signs are assessed.

  • RR: 16
  • Pulse: 116
  • NIBP: 115/53
  • SpO2: 96 on RA

Breath sounds clear bilaterally.

Neuro exam: No facial droop, equal smile, clear speech. Slight pass pointing on the right side.

The cardiac monitor is attached which shows sinus rhythm, borderline sinus tachycardia.

A 12-lead ECG is captured.

What is your impression of this ECG?

See also:

90 year old male CC: "Possible stroke" – Conclusion

90 year old female CC: Seizure – Conclusion

9 comments

This is the conclusion to 90 year old female CC: Seizure. Be sure to start there first!

When we left off, we had completed our initial assessment of a 90 year old patient who, based on bystander accounts, had a seizure. She is pale, cold to the touch, and feels lethargic.

During our assessment she had an increase in her pulse rate and a 12-Lead ECG was obtained:

This is a wide complex tachycardia at a rate of about 200. Our differentials include ventricular tachycardia, SVT with aberrancy, and preexcited wide complex tachycardia from Wolff-Parkinson-White. Regardless, all wide complex tachycardias should be treated as V-Tach until proven otherwise!

When I first saw this ECG, I found the computerized interpretation very interesting because it is almost 100% incorrect.

A quick look at the measured rate shows the cardiac monitor's interpretation cannot be trusted. Using the big block method, the rate is between 150 and 300 bpm, and when calculated is around 206 bpm.

Additionally, the cardiac monitor believes the rhythm to be atrial fibrillation with a rapid ventricular response. However, as many of our astute readers noted, this is clearly ventricular tachycardia

An initial R-wave in aVR is over 98% specific for ventricular tachycardia1!

Based on Patrick J. Lynch's medical illustration; Creative Commons Attribution 2.5 License 2006

If we look at lead aVR, we see the ventricles are depolarizing towards this lead. Clearly this cannot be a supraventricular rhythm such as atrial fibrillation or SVT. In those cases the initial axis will nearly always point away from aVR.

The paramedics in this case correctly diagnosed ventricular tachycardia as well, and began their treatment in the field.

They initially administered 100 mg of lidocaine, however, it had no effect.

Next they elected to use synchronized cardioversion and premedicated the patient with 20 mg of etomidate.

A synchronized shock of 100 J was administered, while the patient was sedated, with a return of a sinus rhythm. A post-conversion 12-Lead was obtained:

This 12-Lead ECG shows a sinus rhythm with a 1st degree AV block and PVCs. There does not appear to be evidence of a STEMI, electrolyte disturbances, or pre-excitation from WPW.

The patient was packaged and had an unremarkable transport to a nearby hospital. The patient was admitted for observation and discharged without incident.

This case highlights a few key points:

  1. The computerized interpretation is no substitute for a human's interpretation.
  2. Wide complex tachycardias should be treated as ventricular tachycardia in the field.
  3. An initial R-wave in aVR is diagnostic of ventricular tachycardia.

What are your thoughts on the case?

[1] Vereckei A, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm; 2008 (5): 89-98.