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17 year old male CC: Syncope

53 comments

EMS is called to a local restaurant on a very hot day for a 17 year old male patient who experienced a syncopal episode.

On arrival the patient meets the ambulance in the parking lot and says, "Hey, man, I'm really sorry. We don't need the ambulance." 

Paramedics asks what happened and he says, "I just sort of… you know… took a hard swallow of Mellow Yellow… I guess…. and…. like…. I don't know if it went down wrong…. or whatever…. but like…. I sort of passed out…. but it's cool now."

The paramedics confirm that the patient is only 17 years old and inquire as to whether or not a parent or guardian is present. The patient's mother steps up and paramedics persuade her to allow them to "check her son out" in the back of the ambulance to "make sure everything is okay" on the condition that they don't receive a bill.

The patient also consents.

In the back of the ambulance the patient states that he is perfectly healthy. The only medical history is acne for which he takes a prescription medication but he forgets the name.

He appears well. The skin is pink, warm and dry.

He states that he has been drinking lots of fluids and making lots of urine.

(In response to one of the comments: he was specifically asked about his fluid status because the weather was hot and humid and EMS had been responding to many heat-related emergencies. This was not intended to convey in any way that the patient is an undiagnosed diabetic).

Both the patient and the mother deny any family history of syncope, seizures, or unexplained sudden deaths.

Vital signs are assessed.

  • RR: 16
  • Pulse: 90
  • BP: 127/84
  • SpO2: 100 on RA

Breath sounds clear bilaterally.

Neuro exam normal.

(Update: The BLG was 108.)

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient says, "So, am I going to live?"

What are your thoughts?

See also:

17 year old male CC: Syncope – Discussion

Posted by on July 30, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , ,

63 year old male CC: Shortness of breath – Conclusion

7 comments

This is the conclusion to 63 year old male CC: Shortness of breath. You may wish to go back and read the original post.

Let's take another look at the 12-lead ECG.

Now with the computerized interpretation.

This ECG shows severe left ventricular hypertrophy with a "strain pattern" or secondary ST-T wave abnormality.

A "strain pattern" often shows what I sometimes refer to as "pouty-lipped" ST-depression and T-wave inversion in the lateral leads. You can see a good example of this in leads I and aVL.

The Q-wave in lead aVL looks suspicious. However, when the patient's chart was pulled at the hospital it turned out that the patient had a history of myocardial infarction.

In addition, ST-elevation is present in the right precordial leads (V1-V3). This is normal for left ventricular hypertrophy. Typically, the deeper the S-waves the more pronounced the secondary ST-T wave abnormality in the opposite direction.

In this case the most pronounced ST-elevation is in lead V2 and you will note that the S-waves are at least 35 mm in this lead (which meets the LVH voltage criteria all by itself). With a "strain pattern" like this the ST-elevation is usually, but not always, upwardly concave.

This patient was suffering from a new onset of acute pulmonary edema and clearly has a very sick heart but ruled out for acute myocardial infarction.

According to some studies LVH is the most common cause of ST-elevation in chest pain patients so this is an ECG abnormality you should learn and keep in the back of your mind! 

Interestingly, it's not easy to find an ECG that shows acute anterior STEMI and concomitant left ventricular hypertrophy in the precordial leads. Stephen Smith, M.D. from Dr. Smith's ECG Blog has a theory that acute anterior STEMI may attenuate the voltage of the S-waves in the right precordial leads (V1-V3).

You can see a possible example of this phenomenon here: 55 year old male CC: Chest pain. I have a suspicion this ECG from the Cardiphile blog shows the same thing (ignore the fact that it says inferior wall infarction).

The take-home point is that very deep S-waves in the right precordial leads should make you question the diagnosis of acute anterior STEMI.

That's not to say that the patient may not be experiencing acute myocardial infarction! That can happen (we are contantly being told) with a perfectly normal looking ECG. Rather, I am saying that it's probably not an acute STEMI, and that's the relevant point for paramedics and physicians in the emergency department who need to make a decision about activating the cardiac cath lab.

As a final point, someone pointed out a significant change between the rhythm strip and the 12-lead ECG in lead III for this case. That's true, but keep in mind that the rhythm strip was captured in "monitor mode" where the low frequency / high pass filter was set to 1 Hz! The 12-lead ECG was captured in "diagnostic mode" with the low frequency / high pass filter set to 0.05 Hz. To get accurate ST-segments you need to be in diagnostic mode.

See also:

Left ventricular hypertrophy – Part I

Left ventricular hypertrophy – Part II

Posted by on July 27, 2011 • Filed under: Uncategorized • Tagged: , , , , , , , , , , , ,

Part 2 of the Conclusion to 15 year old male CC: fall from vehicle

6 comments

This is Part 2 of the conclusion to 15 year old male CC: fall from vehicle. Be sure to read Part 1 of the conclusion to 15 year old male CC: fall from vehicle to catch yourself up!

Before we find out the answer, let's recap the specifics:

  • 15 year old male thrown from the bed of a pickup truck potentially at 45 mph
  • Unremarkable findings aside from bruising to lower extremities
  • No apparent chest trauma
  • Asymptomatic patient
  • More P-waves than QRS complexes on the 3-lead and 12-lead
  • Unremarkable history

As many of our readers pointed out, there exists some high degree AV block, whether it is a 2:1 AVB or a 3rd Degree AVB there was some disagreement.

The paramedics involved in this case had a similar disagreement and the ED staff did as well. Ultimately, a diagnosis of AV dissociation with an AVB of at least 2nd Degree was made and the patient was referred to a pediatric cardiologist.

Going back to the strips, some degree of AV dissociation is clear, and I've provided the following highlighting to one of the 3-leads:

The question then remains, what was the cause of the AV nodal disturbances? Many readers pointed out some very good possibilities, which I'll list below:

  • Traumatic etiology, likely myocardial contusion
  • Lyme disease from a recent tick bite
  • Congenital AV nodal abnormality

Exploring a traumatic etiology we have to reconcile our patient assessment with the mechanism of injury. Our findings are not suggestive of a traumatic cause. A pediatric patient with a new onset heart block secondary to trauma is not likely to be asymptomatic.

A review of the literature reveals multiple case studies of traumatic causes of heart block, however, every single patient had physical exam findings suggestive of myocardial contusion. I believe we can confidently place a traumatic etiology low on the list of probable causes.

A few readers pointed out Lyme disease, which is a common cause of AV nodal disturbances in otherwise healthy individuals. The carriers of this are Deer Ticks infected with the bacteria Borrelia burgdorferi with an overall incidence of 6 in 100,000 in the US. Findings include a bullseye rash, known as erythema migrans, arthritis, AV nodal disturbances, and a multitude of neurologic findings.

Erythema Migrans by Hannah Garrison licensed under CC-BY-SA-2.5

Given no rash upon physical examination and without clear evidence of a tick bite, it seems unlikely to be the cause. It may be prudent, however, to perform blood tests for B. burgdorferi if no other likely diagnosis exists.

Finally, we come to a congenital abnormality of the AV node, manifested as a high degree AV block with a junctional escape rhythm. Literature reports approximately 1 of every 20,000 to 25,000 live births are associated with some degree of congenital complete AV block (CCAVB).

Interestingly enough, patients have been known to survive beyond 60 years without intervention. In CCAVB, the body compensates for the decrease in heart rate with an increase in stroke volume. Therefore, given a functioning junctional escape rhythm, a patient may have no symptoms associated with their cardiac rhythm.

However, these patients often experience syncope or Stokes-Adams attacks usually due to uncompensated bradycardia. If left undiagnosed, their abnormality may only be found on autopsy after a sudden cardiac arrest. Follow-up with monitoring of patients diagnosed with CCAVB is important to identify the need for permanent pacemaker implantation. Any incidence of CHF, persistant bradycardia, or syncope indicates the need for definitive management.

So what was our patient's diagnosis?

The paramedics involved in this case relayed that a diagnosis of congenital complete heard block was made and the patient was scheduled for monitoring for possible pacemaker implantation.

References

  • Athreya BH, Rose CD. Lyme Disease. Cur Prob in Ped 1996; 26:189-207.
  • Dedeoglu F, Sundel RP. Emergency Department Management of Lyme Disease. Clin Ped Emerg Med 2004; 5:54-62.
  • Surawicz B, Kilans T (eds.). (2008) Chou's Electrocardiography in Clinical Practice: Adult and Pediatric (6th ed.). Saunders, Elsevier Health Scences.
  • Michaelsson, M. Congenital complete atrioventricular block. Prog in Ped Cardio 1995; 4:1-10. 
Posted by on July 24, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

63 year old male CC: Shortness of breath

16 comments

By request I'm trying something new. The 12-lead ECG will be cropped and the computerized interpretation removed until the solution is posted. Let me know if you find this approach to be useful. This is how I used to teach 12-lead ECG interpretation but I started leaving the computerized interpretation because that's reality — you'll have access to it in the field (unless you're one of those few systems that turns the comptuerized interpretation off).

EMS is called to the residence of a 63 year old male with a chief complaint of shortness of breath.

On arrival the patient is found sitting on the edge of his bed. He appears to be in moderate respiratory distress.

Past medical history: HTN, IDDM, CHF

Medications: Numerouos (the spouse hands you a large plastic container full of medications)

On questioning the patient admits that he is also experiencing chest tightness.

  • Onset: 30 minutes prior to EMS arrival
  • Provoke: Symptoms are worse lying flat
  • Quality: "Tightness"
  • Radiate: The sensation does not radiate
  • Severity: 5/10
  • Time: Patient admits to prior episodes.

A prolonged expiratory phase is noted.

Breath sounds: basilar rales

Vital signs are assessed.

  • RR: 26
  • Pulse: 80
  • BP: 179/92
  • SpO2: 84 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

By request here are the computerized measurements:

  • HR: 78
  • PR: 206
  • QRS: 104
  • QT/QTc: 430/490
  • P-QRS-T:  23  -39  159

What is your interpretation of these ECGs?

How would you treat this patient and why?

Posted by on July 23, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

ECG Challenge – Is it a STEMI?

41 comments

Since you all seemed to enjoy the link I posted to the ACC's ECG Challenge from 2006 I thought I'd give you another ECG Challenge.

I'm working on a special project (details to be announced soon) and I came across this interesting ECG from the archives of an old computer.

I thought it was long lost! At least the original un-cropped version.

This is one of the very first ECGs transmitted across our first LIFENET system (many years ago).

Let us assume that the patient is experiencing signs and symptoms consistent with ACS.

Does it show acute STEMI? No cheating if you've seen this before! 

(Note: Lead V4 is in the position of lead V4R.)

Posted by on July 21, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

Part 1 of the Conclusion to 15 year old male CC: fall from vehicle

37 comments

This is Part 1 of the conclusion to 15 year old male CC: fall from vehicle.

Lots of great comments, including an unexpected sidebar discussion on appropriate C-spine clearance! All of our cases on EMS 12-Lead have been altered from their original form to protect patient and provider privacy and it appears I changed things enough to give a different focus. So let's quickly touch on the consideration of spinal immobilization in this case.

Given an alert and oriented patient, normal neurological exam, negative pain to the C-/T-/L-spine, no distracting injuries, and no intoxication, it is not unreasonable to forgo immobilization in this patient. When our story contradicts our patient presentation, we should find the middle ground. Given our physical findings consistent with a more moderate mechanism an unstable spinal injury is unlikely. Yet, given provider suspicion it is also not unreasonable to place this patient into spinal immobilization. I think you can sell it either way.

However, the patient presentation in this instance was meant to be a distraction for our readers! Let's revisit the first strip to see why:

We've only got one lead, and as some commentors noted there is a lot of artifact. However, lead II has some clear parts with interesting findings that one of the crew members marked up!

We can see regular atrial activity and regular ventricular activity, yet it seems off. Many readers pointed out the likely cause is a 1st Degree AVB with artifact. Based on this strip alone that is the most reasonable explanation. However, as everyone pointed out, it would be prudent to get a cleaner strip and a 12-Lead to confirm our suspicion.

At first glance, our next strip points to uncomplicated 1st Degree AVB. However, as one of my instructors often pointed out, "the PR-interval will not progressively shorten." A closer look at the second strip shows a progressively shortening PRi which eventually prolongates again!

This cannot be an uncomplicated 1st Degree AVB.

By our third strip it is obvious we have something more than a simple prolonged PRi. Leads II and III show hidden P-waves marching out from underneath the QRS complexes. We now have more P-waves than QRS complexes, leaving us with at least a 2nd Degree AVB or a 3rd Degree AVB.

The next two strips were sent in but not included in the original discussion, however, I hope they foster additional discussion as to which high-degree AV block is present.

In the above strip, compare leads II and III closely. Contrast that with your findings in the below strip:

  • Given our findings does the argument for a 1st Degree AVB still stand?
  • Is a 2nd Degree AVB or 3rd Degree AVB present? Could both be present?
  • If it is a 3rd Degree AVB is it complete or is there occasional capture?
  • Is it reasonable that our patient's traumatic injury is the cause of these isolated findings on the ECG?
Posted by on July 19, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , ,

15 year old male CC: fall from vehicle

45 comments

It has been a busy afternoon as the local schools are out for the Thanksgiving holiday. You've shift traded to get a longer vacation and are working with a newer paramedic. It's not long after dinner when you're paged out for a motor vehicle collision with an ejection.

The details are hazy, but first responders on scene report a young man was thrown from the bed of a small pickup truck.

As you arrive, you notice the pickup truck involved appears undamaged and a crowd has gathered along the curb. You're met in the road by the officer from the engine company who tells you, "the kid was lucky, seems fine; thrown from the bed after they hit a pothole."

The facts appear to be that the pickup was traveling around 45 mph when it struck a pothole throwing the patient–who was sitting in the bed on the wheel well–out onto the street, remarkably landing on his backside without incident.

Your partner passes you and begins his patient assessment. 

  • Conscious, alert and oriented to person, place, time, and event
  • Answers all questions appropriately and without hesitation
  • Denies neck or back pain, no pain to palpation of C-/T-/L-spine
  • Pain to palpation of left knee, thigh and hip without deformities, crepitus, shortening, or rotation
  • Good pulse, motor, and sensory function in all four extremeties
  • Denies alcohol or drug use

He concludes spinal immobilization is not necessary and directs a first responder to let go of manual inline stabilization.

The patient's father has arrived on scene and asks that he be taken to the local hospital for further evaluation. The engine company helps lift the patient to your stretcher and secure him for transport.

Your partner says, "I've got this," and you begin routine transport to the local ED. Vitals are obtained in the back of the unit.

  • HR: 60, regular
  • BP: 118/72
  • RR: 18, unlabored
  • SaO2: 100% on r/a

A further interview reveals no past medical history, no medication usage, NKDA, and only seasonal allergies.

Given the routine nature of the transport, you're a bit suprised to see your partner's head appear in the pass-through holding a 3-Lead, "does this look funny to you?"

At the next stop light, you take a quick look at the strip and ask to see another. He hands you a second strip.

A pile of strips is forming on the bench seat while the car behind you honks impatiently, he continues, "here is the weirdest looking one!"

His next question is short, "should we divert?"

Update 18 July 2011 17:24 EST

As you arrive at the ED your partner hands you the following 12-Lead.

  • What do these rhythm strips show?
  • What does the 12-Lead show?
  • Is there cause for concern?
  • Does this patient require immediate treatment?
  • Do you divert from the local ED to a larger hospital with specialists?
Posted by on July 18, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , ,

Conclusion to “41 Year old female: chest pain”

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This is the conclusion to 41 year old female: chest pain.

I think we would all agree the patient presentation is suspicious for ACS. Let's review the first 12 Lead:

The rhythm is sinus tach. There is about 1mm of ST elevation in V1, and depending on where you spot your J point, little to no elevation in leads V2, V3.  There is about 1mm of ST depression in leads I, II, and V6.  Lead III also has a Q wave and an inverted T wave.  However, both a Q wave and an inverted T wave in lead III may be normal.  One could definitely argue this is a suspicious looking 12 Lead, but I'm not sure if any of us would activate the cath lab based on this ECG alone.  If serial ECG's are not done, the cath lab is not activated, and likely nothing will be discovered to change that.

But, you are all well aware of the importance of serial ECG's, and so was the Medic on this call.  So let's take a look at the second 12 Lead, taken only 7 minutes later:

There are obvious dynamic changes here.  For starters, there are now hyperacute T waves that tower over the QRS in leads V2 and V3, and are much larger than they were in V4.  They are localized to leads V2-V4 and "point" to the area of infarct. The ST elevation in leads V1 and V2 is now 3mm, and in V3 is 3-4 mm. The ST depression in leads I, II, and V6 have deepened slightly.  The T wave inversion in lead III has deepened, and there is now measurable ST depression in aVF.  Also, there is subtle loss of the R wave in leads V2-V3.  On its own, this ECG is probably diagnostic of STEMI, but with the dynamic changes compared to the first one, it is virtually assured.

In the third 12 Lead:

The hyperacute T waves are not as towering as they were…the ST elevation in V1-V3 are now 1-2mm, and the ST depression has greatly resolved.  The inverted T wave in lead III is now mostly upright.  These changes are likely the result of the treatments given by the Medic, perhaps some reperfusion of the culprit artery.

To illustrate how dynamic these changes were over the course of the three ECG's, have a look at leads V1-V3 side by side:

At the cath lab, the patient was found to have an occlusion of the LAD, for which she was stented.

Some key points to take away:

  • The importance of serial ECG's can not be overstated.
  • Subtle changes,such as straightening of the ST segment or subtle enlargement of the T wave may be the first change on the ECG.
  • Hyperacute T waves are localized, and "point" to the area of infarct.
  • ST deviations may normalize after treatments such as ASA, NTG… Failure to do serial ECG's may delay patient care if these deviations are missed. For additional information on this point, see this excellent post on Dr. Smith's ECG Blog.

 

 

Posted by on July 15, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , ,

Automated compression device war turns hardcore

22 comments

I received an email from a ZOLL rep this morning that had a file attachment called "AutoPulse Technical Report #3".

The report shows a crash test with a mannequin outfitted with either the AutoPulse or the LUCAS compression device.

Wouldn't you know it? The LUCAS device lost.

Ladies and gentlemen: the gloves are off!

Posted by on July 12, 2011 • Filed under: ems-topics, patient-management • Tagged: ,

How much should an ear ache cost?

8 comments

Photo credit: Kelly Arashin

I had a very relaxing and restorative trip up to northern Michigan last week with my family.

The weather was perfect. There was sightseeing in national forests, campfires and s'mores, good wine, good stories, and some hard work constructing a drainage system on the side of my parents' log home on Lake Huron.

However, one little aspect of my trip wasn't so nice: an earache.

I've suffered from occasional earaches since I was a little kid. For whatever reason I have small, tortuous ear canals which are susceptable to occasional infections, especially when I swim in a lake or the ocean.

Since I've been dealing with earaches for a very long time I know exactly how to treat them. I irrigate the infected ear with 50/50 water and hydrogen peroxide and I apply Cipro ear drops twice daily until the infection is resolved (which doesn't take long at all provided that I'm not out of Cipro ear drops).

Well, wouldn't you know it, I didn't bring Cipro ear drops with me on vacation. I didn't have a 10 or 20 cc syringe either. So I did what anyone else would do under the circumstances.

I toughed it out until I got home.

Unfortunately, when I got home I couldn't find any Cipro ear drops. So I either lost them or I'm out.

I did, however, irrigate my infected ear and gently applied triple antibiotic ointment with a Q-tip (I know, I know — listen, I was desperate).

To make matters worse, my regular doctor recently moved his practice a couple of hundred miles away to be closer to his aging mother. I have a new doctor who saw me recently for knee pain. Nice guy, but I don't know him well.

So here's my question to all of you. Is it reasonable that I should have to drive 30 miles, sit in the waiting room, get shuffled back into an exam room, get my vital signs taken, receive a physician exam, obtain a prescription, and get billed for a $60-$100 office visit, just to get a prescription for medical problem that I've had for my entire life?

I'm hoping that won't be necessary. I called the new doctor's office and spoke to an office clerk. I explained the situation and requested that a prescription be called into my local pharmacy. She seemed less than enthusiastic but told me that a nurse would call me back later with the doctor's reply.

Posted by on July 12, 2011 • Filed under: Uncategorized

41 Year Old Female: Chest Pain

39 comments

Here's an interesting case sent in by faithful reader Carl R. Christiansen, Paramedic, from Norway. As usual, changes have been made to protect patient confidentiality.

It's an early Sunday morning when you are dispatched to a hotel for a 41 year old female with chest pain. 

You and your partner enter the hotel room and find the woman lying in bed.  As she sits up to greet you, you notice the color of her face is pink, but she seems to be slightly uncomfortable and restless.  She tells you that she woke up at about 8 am with chest pain in the center of her chest, which does not move anywhere.  She isn't short of breath or lightheaded…no nausea or vomiting, or anything else out of the ordinary other than the chest pain.  The pain doesn't change with breathing, movement, or palpation.  She adds that she's had some similar pain come and go over the last three or four days, but never as bad as this.  You ask her to rate her discomfort, and she tells you 9/10.

As you assess her appearance, you don't see anything abnormal… no JVD, no edema.  Her pulse feels rapid but regular, and her lung sounds are clear bilaterally.  Inspection and palpation of her chest and back are normal.  You do a FAST screening, which shows nothing abnormal.  All she can tell you is that she had a couple of glasses of wine with dinner the night before, and slept through the night until the pain woke her up this morning..  She has no relevant medical history, and takes no medications.

While you are getting the history, your partner takes a set of vitals:

  • Pulse:   104 and regular
  • BP:        210/155
  • RR:       18 and regular
  • CTC:     Pink, warm and dry
  • SpO2:   99%

You acquire the following 12 Lead ECG:

What do you think? What would you do next?

The treating paramedic gave the following treatments:

  • One SL NTG
  • 300 mg ASA
  • IV established
  • 2.5 mg of Morphine IV
  • 600 mg Plavix orally

As the above are being done, a second 12 Lead is acquired:

After the treatments were given, the patient's blood pressure dropped to 129/84, and her heart rate dropped to and remained at about 80. The Paramedic called a Code STEMI and transported the patient to a PCI center.  Upon arrival there, this last 12 Lead was acquired by the crew:

What do you see on these 12 Leads?

Would you have called a Code STEMI?

What would your treatment have been for this patient?

 

 

 

Posted by on July 4, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , ,

64 year old male CC: Indigestion – Discussion

11 comments

This is the discussion to 64 year old male CC: Indigestion.

If you recall, we had a stubborn gentleman complaining of indigestion with a significant cardiac history. Considering the symptoms kept our patient awake, are highly suggestive of a coronary event, and we have uncompensated hypotension, we should have a keen interest on any ECG findings.

The rhythm appears to be regular, sinus in origin, rate of ~70 bpm, without ectopy. There is a fixed PR-interval of 0.2 s and a 1:1 association of P-waves to QRS complexes. The QRS is wide at 0.18 s, likely due to a bundle branch block. Normal sinus rhythm with a bundle branch block.

Evaluating the QRS complex in V1, we see it is wide and V1-positive confirming our suspicion of a bundle branch block. However, given the changes in leads I and V6, it is not a classic Right Bundle Branch Block. Instead we have a non-specific intraventricular conduction defect, or IVCD. A right axis deviation is present.

Looking at the contiugous lead groups:

  • Inferior: pathologic Q-waves present, isoelectric ST-segments, non-specific T-wave abnormalities
  • Septal: baseline wander, minimal ST-depression in V1-V2 (potentially attributed to the baseline)
  • Anterior: pathologic Q-wave in V4, isoelectric ST-segments, non-specific ST-T-wave abnormalities
  • Lateral: pathologic Q-wave in V5-V6, isoelectric ST-segments, non-specific ST-T-wave abnormalities
  • High-Lateral: unremarkable outside of underlying conduction defect
  • aVR: unremarkable outside of underlying conduction defect

Pathologic Q-waves in the inferiolateral lead groups are consistent with our patient's history of multiple prior MI's, however, without a prior ECG it is tough to determine if these are not from a recent myocardial infarction.

The potential ST-depression in the septal leads may be reciprocal changes in the setting of a posterior MI. The patient's skin condition made acquisition difficult, but coupled with the patient's signs and symptoms it would be prudent to explore this possibility. Attempts could be made at the acquisition of a posterior view.

The interventricular conduction defect present may be an acute finding or it may be a baseline finding. Given the QRSd is around 0.18 s there is a non-trivial defect present. Without access to the patient's prior ECG's we are unable to determine its significance.

While examination of the 12-Lead ECG for this patient did not yield any acute findings, in conjunction with our patient assessment we have enough to form a differential diagnosis:

  • Acute myocardial infarction
  • Recent myocardial infarction
  • Congestive heart failure
  • Pulmonary embolism (albiet less likely due to symptoms)

However, any differential diagnosis for this patient is rendered moot by his stubborn desire to refuse transport!

The paramedics on this call rolled up their sleeves and got to work convincing this gentleman that his signs and symptoms were anything but normal. He begrudingly sat on the stretcher and consented to transport.

They placed him on O2 by nasal cannula, obtained IV access, administered a fluid bolus, and transmitted the 12-Lead ECG to a local STEMI receiving center. His blood pressure improved enough with fluid administration to allow nitroglycerin, which the patient said improved his discomfort.

Transmission of the patient's ECG was key in this case as the receiving facility determined acute changes were present.

The patient was taken directly to the cath lab where a 90% occlusion of the LAD, just proximal to a previous stent, was found. The lesion was ballooned and stented, and the patient was admitted to the CCU for recovery.

Some additional questions for discussion:

  • Why was this patient's hypotension uncompensated?
  • Are there any differentials we missed?
  • Why was indigestion left off the list of differentials?
Posted by on July 1, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,