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63 year old male CC: Syncope

30 comments

EMS is called to the home of a 63 year old male who has experienced a syncopal episode.

On arrival the patient is found sitting in a dining room chair that his spouse brought to the foyer. A grocery bag is up-ended with groceries all over the floor.

The patient has vomited but he does not appear to be incontinent of urine.

He appears to be acutely ill.

The patient is awake and oriented to person, place, and time but not event.

Skin is cool, pale, and diaphoretic.

The patient’s baseline SpO2 is 96. He is placed on oxygen via NRB mask @ 15 LPM.

He denies chest discomfort, palpitations, or shortness of breath.

Past medical history is significant for hypertension and congestive heart failure.

Medications include aspirin, spironolactone, and carvedilol.

Vital signs are assessed.

RR: 20
HR: 64 R
BP: 102/58

The cardiac monitor is attached.

A 12-lead ECG is captured.

What’s next?

See also:

63 year old male CC: Syncope – Conclusion

Posted by on September 30, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

60 year old female CC: Dizziness – Discussion

4 comments

Let’s talk about this heart rhythm a little bit, and when we do, let’s go back to the basics.

Is it regular or irregular?

It’s irregular.

Is it regularly irregular or irregularly irregular?

It’s irregularly irregular.

Does it have narrow QRS complexes or wide QRS complexes?

It has narrow QRS complexes.

Sight unseen, this heart rhythm has a high probability of being atrial fibrillation. However, wandering atrial pacemaker or multifocal atrial tachycardia is also part of the differential diagnosis.

Is the rate over 100?

Yes.

So is this atrial fibrillation with rapid ventricular response or multifocal atrial tachycardia?

Let’s look at the isoelectric line. Does it appear fibrillatory?

No.

We see atrial complexes before the QRS complexes. However, the P-wave morphology is not constant.

When you have 3 or more distinct P-wave morphologies, you are justified in calling a rhythm like this multifocal atrial tachycardia.

Now, I will tell you that on the cardiac unit a rhythm like this is often referred to as either atrial fibrillation or sinus tachycardia with frequent multi-focal PACs, but that is not correct.

Next, let’s look at the T-waves, because with a rhythm like this it can sometimes be difficult to differentiate P-waves and T-waves.

To find real T-waves, let’s only pay attention to cardiac cycles at the end of clusters of QRS complexes.

This should give you some idea as to the actual amplitude of the T-waves in lead II as well as the QT interval. Once you make a mental note of this, you can go back and decide if the other complexes are T-waves or P-waves superimposed on T-waves.

Now it should be obvious that the cardiac cycle circled in red is showing a P-wave masquerading (isn’t that a ridiculous word?) as a T-wave, whereas the cardiac cycle circled in blue shows an actual T-wave unspoiled by a mega P-wave.

Incidentally, these tall, pointy P-waves in lead II suggest significant right atrial enlargement. Remember, enlarged atria are not happy atria. They are predisposed to various arrhythmias like atrial fibrillation, atrial flutter, and multi-focal atrial tachycardia.

Granted, if you look at the 12-lead ECG, a right axis deviation is not present (right atrial enlargement and right ventricular hypertrophy go together) but the patient’s history includes “severe heart failure” which means that the patient’s entire heart is enlarged, not just the right side.

So what we see is “low voltage” in the limb leads (all QRS complexes < 10 mm), the result of electrical forces on the right and left side canceling each other out.

Especially with the history of COPD, I would call this a pulmonary disease pattern.

So how about the final rhythm strip showing a very fast narrow complex tachycardia?

This is where it’s nice to monitor a patient’s heart rhythm inside the hospital as opposed to inside the ambulance!

If you see a rapid heart rate inside the hospital you can “go back” in time and examine the onset of the arrhythmia to see whether or not it has a paroxysmal (sudden) onset. That would narrow it down to atrial flutter or some kind of reentrant tachycardia.

On the other hand, if the heart rate histogram shows a gradual increase in heart rate that maxed out at 216 you know it’s an automatic focus tachycardia for which adenosine would not be helpful (for example).

This particular arrhythmia turned out to be “self limiting” but even noting the termination of a tachycardia can be helpful in the diagnosis.

Did it stop abruptly (paroxysmal) or did it slow down gradually, revealing flutter waves (again, for example).

Since the patient’s chief complaint of dizziness seems to correlate with this rapid heart rate, definitive care for this condition will take place inside the hospital, and possibly the EP lab.

Sometimes the medications used to control rapid heart rates aren’t desirable for a patient with severe heart failure. Other times, they’re already taking these medications for the heart failure, but they’re experiencing rapid heart rates anyway!

I remember one patient with chronic AF who ultimately required RF ablation of the AV node and a pacemaker!

The atria continued to fibrillate but rapid ventricular response was no longer possible due to surgically induced third degree AV block. That was all the way back in 1997! Still pretty cool.

Thanks for the case, Mark!

See also:

60 year old female CC: Dizziness

Posted by on September 24, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , ,

60 year old female CC: Dizziness

24 comments

Here’s an interesting case study from the Right Honorable Mark Glencorse of Tyneside. In addition to being a founding member of EMS 2.0 and the Chronicles of EMS, he also hosts the popular ECG Geek series at 999Medic.com.

Here is the situation (and no, I’m not talking about Mike Sorrentino).

Called to a 60 yr old female patient. She had been suffering with dizzy bouts and collapses for a couple of weeks and had been diagnosed with vertigo.

Has a medical history of MI (with cardiac arrest) in 2009, severe heart failure, COPD with home O2 via NC @ 2 LPM 24hrs per day.

She called 999 as she felt her dizzy bouts were getting worse and the medication that had been given to her for the vertigo was not working.

On arrival she was dyspnoiec (although in her normal state), slightly pallid and feeling dizzy. No chest pain.

Observations :

GCS: 15
Resps : 32, use of accessory muscles
SaO2: 95% on 2 litres/min O2 via nasal cannula (all normal for her)
Pulse: 92, irregular and weak radial pulse
BP: 102/55

Skin was warm to touch and dry.

She complained that her dizzyness was worse today and that sometimes she felt as though she was falling even when she was lying in bed.

Whilst completing my assessment, my partner rechecked her blood pressure and mentioned that her pulse had gone very irregular and she seemed bradycardic.

A rhythm strip was taken.

Chest electrodes were applied and a 12 Lead ECG was captured.

Patient was moved to the ambulance via carry chair and once on the stretcher called out to say that she had gone dizzy again. Leads were immediately attached to the monitor again which showed the following rhythm strip.

What do you think of these ECGs?

See also:

60 year old female CC: Dizziness – Discussion

Posted by on September 21, 2010 • Filed under: ems-topics, patient-management • Tagged: , , ,

47 year old female CC: Chest pain – Discussion

1 comment

Thanks for all the comments! I’m not allowed to blog while I’m on duty (the policy has nothing to do with me personally) so if it seems like I’m not responding, I’m probably just at work.

The paramedic who submitted this case has requested the follow-up information from his supervisor, but unfortunately she’s out-of-town for the next 2 weeks.

In the meantime, we can lay out the issues.

Obviously, this is a scary looking ECG because there is significant ST-elevation in the precordial leads.

However, this ECG also meets the voltage criteria for LVH.

Could it be a strain pattern (typical secondary repolarization abnormality)?

No.

It’s difficult to tell with the wandering baseline throughout this ECG, but if you line up the point at which the PR-segment hits the QRS complex in leads V1, V2, and V3 you can see that each of these leads shows approximately 4 mm of ST-elevation.

You will recall that with a “strain pattern” the degree of ST-elevation is proportional to the depth of the S-wave in the opposite direction! So the lead with the deepest S-wave should have the most significant ST-T wave abnormality in the opposite direction.

It’s not easy to tell the exact depth of the S-wave because the complexes are running together, but these measurements are probably fairly close.

There’s no way that a typical strain pattern would show the same amount of ST-elevation in one lead with S-waves that are 22.5 mm deep and another with S-waves that are only 6 mm deep.

Here’s the most disturbing finding, in my opinion.

There appears to be reciprocal behavior between the inferior leads and the high lateral leads.

So, if this is a STEMI mimic (for example, benign early repolarization superimposed on top of left ventricular hypertrophy) it’s a darned good one! I wouldn’t blame any paramedic for calling in a STEMI Alert for this patient.

So what should the hospital do when they are in receipt of a patient like this? I asked Stephen Smith MD from Dr. Smith’s ECG Blog and here’s what he said.

“If I were the ED physician, I would aggressively treat the blood pressure with NTG (up to 250 mcg/min or even higher) until the BP came way down. I would do a bedside cardiac ultrasound and look for anterior wall motion. If pain did not go away, and echo did not definitely show good wall motion, I would activate the cath lab.”

It’s always nice to get Dr. Smith’s perspective! I’ve learned a lot from his blog over the past 2 years. If you’re not familiar with his website you should take the time to check it out! His case studies are top notch!

Hopefully we’ll have the outcome in about 2 weeks.

See also:

47 year old male CC: Chest pain

Posted by on September 20, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

Must-see JEMS.com webcast!

1 comment

I came across an outstanding webcast the other day. It’s hosted by JEMS.com and sponsored by Physio-Control. It’s called Connecting Care Teams and Collecting Data: How it helps both you and your patient—The Houston Experience

It’s dated February 18, 2010 so I’m not sure how I missed it the first time around. It will be available until September 20, 2010 at 11:30 a.m.

In other words, you have less than 48 hours!

The presenter is Chris Souders, MD, Associate Medical Director of Houston Fire Department.

This webcast is divided into two parts. The first part is about STEMI and the second part is about cardiac arrest.

The first part features an interesting discussion about the problem of false positives and the value of prehospital ECG transmission. It shows this interesting ECG.

The second part addresses quality assurance of cardiac arrest using the most modern technology available. I was impressed, particularly because my fire department just purchased the new LIFENET technology and CODE-STAT.

Here they use the impedance channel to review chest compressions.

Take a look at the webcast while you can! It’s pretty amazing.

Posted by on September 18, 2010 • Filed under: ems-topics, patient-management • Tagged: , , ,

47 year old female CC: Chest pain

21 comments

Here’s a case study from a faithful reader who wishes to remain anonymous.

EMS is dispatched to a 47 year old female complaining of chest pain.

On arrival paramedics find the patient seated on the floor. She appears acutely ill. Her skin is cool, pale, and diaphoretic.

The patient confirms that she is experiencing severe, sub-sternal chest discomfort.

Onset: 15 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: “Very bad” (language barrier)
Radiate: The pain does not radiate
Severity: 8/10
Time: No previous episodes

She is also complaining of palpitations.

First responders initially suspect symptoms of anxiety based on her young age.

The patient’s son relates that the patient is a diabetic and hands paramedics a bottle of lisinopril and glipizide.

Paramedics ask the patient if she has a history of heart problems. She says “yes” but can not give specifics other than “blood pressure.”

Due to the patient’s poor appearance the EMS crew immediately loads her for transport.

In the back of the ambulance vital signs are assessed.

RR: 18
HR: 80
NIBP: 240/120 (confirmed with manual BP)
SpO2: 97 with NRB @ 15 LPM

Breath sounds are clear bilaterally.

The cardiac monitor is attached and a 12-lead ECG is captured.

What is your impression and what should the EMS crew do next?

Posted by on September 18, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , ,

37 year old male CC: Unconscious – Discussion

7 comments

Here is the follow-up to: 37 year old male CC: Unconscious.

This is the 12-lead ECG that was presented.

There are a few difficulties involved with this case.

First, we have the syncopal episode with possible seizure-like activity and slurred speech.

Second, we have an abormal ECG.

Third, there is a recent history of chelation therapy which may or may not be playing a role in what's happening.

For any patient who experiences a syncopal episode the ECG should be reviewed for high-risk features like cardiac arrhythmias, a prolonged QT-interval, Brugada's syndrome, a Wolf-Parkinson-White pattern, or hypertrophic cardiomyopathy.

Unfortunately, this is an endurance athlete, and it's notoriously difficult (if not impossible) to distinguish between an "athlete's heart" and hypertrophic cardiomyopathy without the aid of an echocardiogram to examine the exact dimensions and shape of the left ventricle.

To me, this ECG clearly shows left ventricular hypertrophy complete with a "strain pattern" (or secondary ST-T wave abnormality).

Remember, left ventricular hypertrophy is considered a "STEMI mimic" and an acute anterior STEMI mimic in particular.

If you're screening the ECG for STEMI and you don't have ST-elevation in the anterior leads, there's no need to measure for the voltage criteria.

Of course, if you've been reading my blog for a while, there's very little reason to measure the voltage criteria if you can identify a "strain pattern".

Consider the following graphics.

ST-elevation is present and the degree of ST-elevation appears to be proportional to the depth of the S-wave. Note that the S-wave is "cropped" in lead V3 by the bottom of the ECG graph paper.

It's worth mentioning that Stephen Smith, MD from Dr. Smith's ECG Blog has stated:

"[I]t is very difficult to find a case of anterior MI with extreme voltage like this; this is probably because profound ischemia of LAD occlusion (STEMI) alters the QRS voltage and attenuates the severity of the electrocardiographic LVH voltage."

It is so rare in fact that he has asked that anyone who has seen an acute anterior STEMI with deep S-waves suggestive of LVH to please contact him! Keep in mind, he wrote the book The ECG in Acute MI.

So, when ST-elevation in the anterior leads is associated with deep S-waves suggestive of LVH, slow down. Take a closer look. You're probably dealing with a STEM mimic!

Now let's look at the lateral leads.

Here again we see "T-wave discordance". In other words, the T-waves are deflected opposite the main deflection of the QRS complex (which is what we're looking for to identify a "strain pattern" with LVH). In addition, the degree of the ST-T wave abnormality is proportional to the size of the QRS complex, but in the opposite direction.

This can sometimes be difficult to appreciate on the prehospital 12-lead ECG because the QRS complexes run together. So take your time and try to identify the true amplitude in each lead.

Finally, take a look at the transition of the T-wave in the precordial leads. By the "transition" I mean the manner in which the T-wave transitions from positively deflected in lead V1 to negatively deflected in lead V6.

As the QRS complex transitions from negative to positive, the T-wave transitions from positive to negative! This is what is meant by "widened QRS/T angle".

If you look at the QRS and T axis at the top of the ECG the QRS axis is 43 and the T axis is 144 which makes the QRS/T angle 101. That's abnormal and suggests T-wave discordance.

So it's clear we're dealing with left ventricular hypertrophy and a strain pattern. Is it "normal" for an endurance athlete? Quite possibly, but it's not our place to make that determination in the field, particularly with the immediate history of syncope.

The best thing the EMS crew did for this patient was take him to the hospital.

If the syncope wasn't reason enough (and in my opinion it most certainly was) the patient had a recent history of chelation therapy. I don't know if the chelation therapy was oral or IV but it doesn't matter. It can contribute to loss of electrolytes and nutrients.

Finally, the slurred speech and loss of clear eye contact. That's what upset the patient's spouse the most, and sometimes we need to stop and listen to the people who know the patient the best. Occasionally this means listening to a mother about about her baby. In this case it means listening to a wife about her husband.

So what was the outcome?

The patient ended up receiving a CT scan of the head at the receiving hospital. A slow venous bleed was discovered. He was transferred to a tertiary care center for more advanced care.

To the best of my knowledge this was the patient's normal ECG.

Update: Here's what electrophysiologist and cyclist Dr. John M had to say about the patient's ECG:

That ECG is very abnormal. Agree with strain diagnosis. Not only that, but the QRS is notched and fragmented. V1's pattern along with the prominent p-wave voltage suggests the possibility of an ASD. I would agree with you entirely about the non-benignness of this patient's syncope, and I would be very interested in the ECHO report.

See also:

Left ventricular hypertrophy – Part I

Left ventricular hypertrophy – Part II

41 year old male CC: Chest pain

41 year old male CC: Chest pain – Answer

Posted by on September 15, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

37 year old male CC: Unconscious

29 comments

EMS is called to evaluate an unconscious 37 year old male.

En route to the scene dispatch advises paramedics that the  patient is now conscious and may have experienced a syncopal episode and seizure-like activity. The spouse believes that the patient may be having a stroke.

On arrival the patient is found lying in bed. He is alert and oriented to person, place and time, but not event.

He appears to be in excellent shape.

The spouse informs the EMS crew that the patient is an endurance athlete who has recently undergone chelation therapy to “clean out his system.” It’s clear this has been controversial topic their relationship. The spouse is not pleased about it.

She is clearly shaken by what has happened and is particularly concerned that the patient slurred his speech immediately after re-gaining consciousness.

The patient states that he was “worked up for chest pain” about 3 months ago and all tests came back negative. Otherwise he states that he has been healthy. He takes no meds.

Vital signs are assessed.

RR: 18
HR: 80 R
BP: 140/90
SpO2: 98 on RA

Breath sounds are clear bilaterally.

BGL: 108

The cardiac monitor is attached.

A 12-lead ECG is captured.

The paramedics sit the patient up to check orthostatics. The patient’s eye contact becomes less focused and his speech becomes slurred. He seems weak.

What are your concerns?

See also:

37 year old male CC: Unconscious – Discussion

Posted by on September 14, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

78 year old male CC: Chest pain – Discussion

5 comments

I posted this case for a few reasons, but not because it was difficult. So if you were looking for a zebra, I’m sorry to disappoint you!

I have noticed on many occasions that a paramedic’s inability to recognize a paced rhythm can lead to incorrect interpretations of the 12-lead ECG. That’s why it’s important to look (and feel) for a pacemaker can when you do your physical exam!

You do perform a physical exam, right? (Say yes.)

When you completely undress your patient from the waist up, it helps with proper lead placement, reveals surgical scars and implantable medical devices, and allows you to assess breath sounds more accurately. It’s just a good habit to get in to.

Let’s look at the 12-lead ECG again.

For this case there are a couple of big tip-offs that we’re dealing with a paced rhythm.

It’s a supraventricular rhythm with a wide QRS complex, left axis deviation, and LBBB morphology in lead V1. This is the most common morphology for paced rhythm and suggests that the pacing lead is in the apex of the right ventricle.

You will also note negative concordance of the QRS complexes across the precordial leads which is suggestive of a ventricular rhythm. Negative concordance of the QRS complex is not always present but it’s a common feature of ventricular paced rhythms.

In addition, pacer spikes (or blips or “nubbins” since Christopher is making up his own words) are visible in a few leads, most notable of which is lead V4. This makes sense when you think about it because lead V4 is in close proximity to the apex of the right ventricle.

This case is also a nice example of appropriate T-wave discordance. Since all of the precordial leads show negative QRS complexes, let’s arrange them smallest to largest and see if we notice anything.

See how the T-wave gets larger and larger as the S-wave gets deeper and deeper? The more times you look at this in a “normal” paced rhythm or left bundle branch block ECG, the easier it will be for you to identify when something looks “wrong”.

I have no idea what was causing this man’s chest pain but I feel confident it wasn’t an acute STEMI.

Speaking of acute STEMI, I was recently made aware of another case where a computer algorithm incorrectly identified a WPW Type B pattern.

This was sent to me by Dr. Jody Griswold.

This is an interesting case in its own right and Dr. Griswold wrote a very informative paper about it which you can download here (with Dr. Griswold’s permission):

WPW_Type_B_versus_STEMI (This is a Word .doc).

Just to show that the GE-Marquette 12SL interpretive algorithm gets it right sometimes,  check out:

Wolf-Parkinson-White (WPW) – STEMI Mimic.

See also:

78 year old male CC: Chest pain

Posted by on September 12, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , ,

78 year old male CC: Chest pain

9 comments

EMS is called to the residence of a 78 year old male.

It’s the middle of the night. The patient’s spouse meets you at the front door and brings you back to the bedroom.

The patient is sitting on the edge of his bed. He is highly anxious and complaining of chest discomfort and palpitations.

Onset: During sleep
Provoke: Running made the sensation feel better earlier the previous day
Quality: An “electric” sort of “full” feeling in his chest
Radiate: The sensation does not radiate
Severity: 5/10
Time: Started earlier the previous day but went away after running

The patient takes several deep breaths during EMS evaluation and seems upset that it doesn’t correct the problem.

Skin is pink, warm, and moist.

Breath sounds are clear bilaterally.

Vital signs are assessed.

RR: 20 and shallow
HR: 100
BP: 160/98
SpO2: 98 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

And another.

What’s going on here?

Could this be WPW?

Why or why not?

See also:

78 year old male CC: Chest pain – Discussion

Posted by on September 11, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

76 year old female CC: Chest pain – Conclusion (Tako-Tsubo Cardiomyopathy)

15 comments

Here is the conclusion to the most recent case: 76 year old female CC: Chest pain.

To see Part I click HERE. To see Part II click HERE.

The patient was transported to the emergency department where she was treated for a possible acute coronary syndrome.

Serial 12-lead ECGs and cardiac biomarkers were performed.

This 12-lead ECG was captured at 1407.

This is fairly similar to the prehospital 12-lead ECGs.

The next 12-lead ECG is from 1722.

This ECG is significantly different from the prehospital 12-lead ECGs.

You will note that the hyperacute T-waves are gone, as are the ST-elevation and reciprocal changes.

Let’s look at the cardiac biomarkers.

1407

CPK……………………….38
CKMB…………………..2.56
Troponin……………..< 0.01

1730

CPK……………………….72
CKMB…………………12.30(H)
Troponin……………..0.562(H)

The patient was admitted to the hospital.

Echocardiogram showed a large anteroseptal wall motion abnormality.

0610 (the following morning)

CPK……………………….48
CKMB…………………..7.46(H)
Troponin……………..0.211(H)

It should be noted that with changes on serially obtained ECGs and a rise and fall of cardiac biomarkers, the WHO criteria for the diagnosis of acute myocardial infarction has been met.

The patient was sent to the cardiac cath lab for PTCA and stents if needed.

Results:

  1. Insignificant epicardial coronary artery narrowing in a right dominant system.
  2. Congenitally absent left main (normal variant).
  3. Severely reduced left ventricular systolic function, left ventricular ejection fraction 35% with a large anterolateral and apical area of akinesis. The apex is aneurysmal.
  4. Likely apical ballooning syndrome versus spasm in the left anterior descending coronary as a cause of the apical wall motion abnormality.

So, what is “Apical Ballooning Syndrome”?

It is also called “Tako-Tsubo Cardiomyopathy,” “Stress Cardiomyopathy,” or “Broken Heart Syndrome.”

“Tako” is the Japanese word for octopus and “Tsubo” is the Japanese word used for pot or trap. The Japanese physician who first described this condition noted that the end-systolic ventriculogram took on the shape of an “octopus pot” and hence the name “Tako-Tsubo” or “Takotsubo”.

Here’s an image that shows a side-by-side of the patient’s ventriculogram (end-diastole on the left and end-systole on the right).



This is a fairly obscure but well documented STEMI mimic (although one article I found from Mayo Clinic Proceedings suggests that spontaneous aborted MI is a more likely scenario).

If you would like to learn more about Tako-Tsubo Cardiomyopathy you can see the Wikipedia article HERE. The eMedicine article is HERE. The Medscape article is HERE.

From the Medscape article:

“Patients often present with chest pain, have ST-segment elevation on electrocardiogram, and elevated cardiac enzyme levels consistent with a myocardial infarction.1 However, when the patient undergoes cardiac angiography, left ventricular apical ballooning is present and there is no significant coronary artery stenosis.”

“One of the more unique features of TCM is the association with a preceding emotionally or physically stressful trigger event, occurring in approximately two thirds of patients.”

“Recently, TCM has been reported after near drowning episodes.“

How about that, Dr. House?

See also:

76 year old female CC: Chest pain

76 year old female CC: Chest pain – The case for this being an acute anterior STEMI

Posted by on September 9, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

76 year old female CC: Chest pain – The case for this being an acute anterior STEMI

9 comments

I find this case to be extremely interesting for a variety of reasons. (Click HERE to see the original post).

As many of you pointed out, the history and clinical presentation isn’t exactly screaming “Acute Coronary Syndrome!”

But then, as others have pointed out, the elderly often have atypical or vague symptoms.

Let’s look at the 12-lead ECG itself (I will post the serial ECGs to the original case study so you can see those, too).

First question, does it meet the ACC/AHA STEMI criteria (imperfect though it may be). I have to admit, when I first reviewed this case I didn’t see it, but the answer is, “Yes.”

Hyperacute T-wave are visible in several leads, the most noticeable of which are leads V4 and V5.

Here’s an important teaching point, courtesy of Dr. Smith from Dr. Smith’s ECG Blog in reference to this case.

“The T-wave is the best indicator of viable myocardium at risk.”

Is ST-elevation also present?

Some of you have been taught that 2 mm of ST-elevation is required in two contiguous precordial leads. That is only the case for leads V2 and V3. This is probably due to the fact that leads V2 and V3 often have deep S-waves.

In this case, lead V4 has about 2 mm of ST-elevation and lead V5 has 1 mm of ST-elevation.

Couldn’t this be benign early repolarization? In theory, yes, although BER is not particularly common in elderly female patients.

There’s also another way to tell. Look at the R-wave progression in leads V1-V4. It’s non-existent, which points away from benign early repolarization.

Do any other leads show ST-elevation?

As some of you mentioned in the comments, ST-elevation is present in the high lateral leads I and aVL. However, it’s less than 1 mm. So it’s not significant. Right?

Wrong.

It’s significant due to the low amplitude of the QRS complex! You have to consider proportionality.

To illustrate this point consider the following graphics that “stretch” leads I and aVL vertically while preserving the ST/QRS ratio.

This is the same image side-by-side but the image on the right has been “stretched” vertically. It’s a single cardiac cycle in lead I. It looks much worse when it’s stretched, doesn’t it? But the ST/QRS ratio is exactly the same!

Here’s another example of lead I.

Here’s lead aVL, normal on the top and “stretched” vertically on the bottom.

If only there were reciprocal changes to firm up the diagnosis!

You will notice a flattening of the ST-segment in leads III and aVF that by itself would not seem particularly significant in a 76 year old female with a history of emphysema. However, it’s all about context! Over and over again I have preached Tomas Garcia, MD’s admonition to “consider the company” that any ECG abnormality keeps.

A flattening of the ST-segments in the inferior leads when the anterior and high lateral leads are suspicious for acute STEMI should be considered reciprocal changes.

Now what do you think? Are you sold or do you still have doubts?

See also:

76 year old female CC: Chest pain

76 year old female CC: Chest pain – Conclusion (Tako-Tsubo Cardiomyopathy)

Posted by on September 6, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

Return of the Geordie

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Just in case you didn’t know, Mark Glencorse (999Medic.com) is back from his hiatus from blogging.

Also, congratulations to Mark on his new column in the Journal of Paramedic Practice (JPP) called Blog Watch! The August 2010 edition is out and Mark was kind enough to include the Prehospital 12-lead ECG blog.

Mark mentions the case study 58 year old female CC: Chest pain which meets all three of Sgarbossa’s criteria for identifying acute STEMI in the presence of LBBB.

Actually, it meets two of the original criteria, but all three if you include the modified criterion of discordant ST-elevation > 0.2 the depth of the S-wave (ST/QRS ratio).

(You know, it hasn’t been all that long since I moved over to FireEMSBlogs.com but my old blog looks sort of ugly, doesn’t it?)

Thanks, Mark! Welcome back.

Incidentally, if anyone wants to learn how to communicate with Mark, click here.

Posted by on September 5, 2010 • Filed under: ems-topics • Tagged: , , , , , , , , , ,

76 year old female CC: Chest pain

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EMS is called to the beach for a 76 year old female complaining of shortness of breath. Past medical history of emphysema.

On arrival, the patient is found sitting in a beach chair alert and oriented to person, place, time, and event. She does not appear to be in any acute distress.

The patient states that she was out wake-boarding when she fell and “got a mouth full of water.” She coughed profusely and then experienced some chest discomfort.

She denies having experienced any shortness of breath.

She denies any other significant medical history other than a little bit of emphysema and states that she takes an inhaler but rarely uses it.

The patient is embarrassed but consents to further evaluation in the back of the ambulance. It takes some convincing for the patient to allow EMS personnel to carry her off of the beach (she wants to walk the 100 yards to the ambulance).

In the back of the ambulance, vital signs are assessed.

RR: 18
HR: 80
BP: 132/74
SpO2: 94 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient states she feels better and wants to know if it’s really necessary for her to go to the hospital.

What should the paramedics tell her and why?

*** Update 09/06/2010 ***

By request, here are the serial prehospital 12-lead ECGs for the case.

See also:

76 year old female CC: Chest pain – The case for this being an acute anterior STEMI

76 year old female CC: Chest pain – Conclusion (Tako-Tsubo Cardiomyopathy)

Posted by on September 5, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,