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Angioplasty with Bezold-Jarisch Reflex

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From the blog of Dr. Wes, check out this BBC news video of a STEMI patient receiving angioplasty. Interesting that he could localize his pain and the quality was “sharp” as opposed to dull. It just goes to show the limitations of the OPQRST for ACS patients. I’m assuming it was the RCA as reperfusion seems to have triggered a run of VT.


Acute inferior STEMI often presents with sinus bradycardia due to the Bezold-Jarisch reflex (or less commonly direct ischemia of the SA node) but anyone who works in the cath lab will tell you that sudden reperfusion of the RCA triggers the reflex in a more dramatic fashion, sometimes putting the patient into VF.

After watching it twice, I noticed that the cardiologist is looking at what appears to be a prehospital 12 lead ECG! Apparently it’s not necessary to repeat the 12 lead ECG in the emergency department after all!

Posted by on January 31, 2009 • Filed under: Uncategorized • Tagged: , , , , ,

SC Chapter of AHA Mission: Lifeline

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I was recently invited to be on the EMS Advisory Committee for the South Carolina chapter of the AHA’s Mission: Lifeline (the AHA’s STEMI initiative).

This is a collaborative partnership between the AHA, South Carolina Hospital Association, South Carolina Chapter of American College of Cardiology, South Carolina Chapter of the College of Emergency Physicians, South Carolina Department of Health and Environmental Control Office of Emergency Medical Services, all 17 of the South Carolina hospitals that provide interventional cardiac services and patient advocate representatives.

The first organizational meeting was held yesterday in Columbia, SC. As luck would have it, I was already in Columbia for the FEMA Structural Collapse Technician Course which concluded one day earlier.

I wasn’t sure what to expect, but I was pleasantly surprised by the professionalism of all involved.

One of the more interesting things about the meeting was identifying the incredible diversity of the various EMS systems across the state.

Some have been doing 12 lead ECGs for over a decade, and have a history of giving prehospital Retavase in the field. Others just acquired 12 lead ECG monitors. A few are still using basic 3-lead cardiac monitors.

Some can transmit 12 leads from the field. Others can’t.

Some have extensive training programs for 12 lead ECGs. Others have limited their training to a couple of hours, citing the difficulty of teaching older paramedics new tricks.

Some have great working relationships with the ED docs. Some don’t.

Some are so rural that no cell signals are available in huge areas of their respective counties.

Some counties have no hospitals.

Some EMS systems are forbidden to take their ambulances out of the county, which means they are limited to delivering patients to facilities incapable of performing primary PCI.

Many EMS sytems are already struggling financially, even without the economic downturn.

These are incredible challenges that need to be overcome. If not for the highly professional people I met yesterday, I might have considered it a fool’s errand. Instead, I feel optimistic.

I sense the tide is really starting to change.

These are interesting times, both for EMS, and for emergency cardiac care.

Posted by on January 30, 2009 • Filed under: Uncategorized • Tagged: , , , , , ,

FEMA Structural Collapse Technician Course

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If you’re wondering why I haven’t posted anything in over a week, it’s because I was away at the South Carolina Fire Academy in Columbia, SC taking the 8-day FEMA Structural Collapse Technician Course.

It consisted of:

  • 3 days of collapse shoring
  • 2 days of lifting and rigging heavy objects
  • 2 days of breaching, breaking, and cutting
  • 1 day of a scenario that combined all skills

The least I can say is, I love me some torches! :)

Posted by on January 30, 2009 • Filed under: Uncategorized

Prehospital 12 Lead ECG – What Are the Indications?

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The primary purpose of the prehospital 12 lead ECG is to detect acute coronary ischemia or injury in the prehospital setting.

That's not to say it's the only purpose for a prehospital 12 lead ECG, but it's the main reason we carry 12 lead monitors on the ambulance!

Ideally, the early identification of STEMI patients will:

  1. Ensure delivery of STEMI patients to facilities capable of performing prompt, expertly performed primary PCI (regional systems of care).
  2. Shorten door-to-balloon (D2B) times by enabling parallel processing, or early activation of the cardiac cath lab, especially during off-hours (nights, holidays, weekends) or anytime the cath lab isn't staffed 24 hours/day.


So which patients should receive a prehospital 12 lead ECG, and why? What are the indications?

I'll start with my top 10, and open it up for discussion.

1.) Chest pain or discomfort – In my opinion, any unusual sensation, nose to navel, front or back, qualifies. This will ensure that you cast a wide net and pick up on lots of atypical presentations.

2.) Shortness of breath – I ask all chest pain patients about shortness of breath (many admit to mild dyspnea even with normal respiratory rates and clear breath sounds), and I ask all shortness of breath patients about chest pain. Both get a 12 lead ECG regardless. Be especially mindful of new exertional dyspnea, particularly in the elderly patient, and acute pulmonary edema.

3.) Syncope or near syncope – Let's face it, a lot of our syncope patients end up refusing transport to the hospital, but a small subset are at high risk for sudden death! Capture a 12 lead ECG and review it for ACS, arrhythmias, a prolonged QT/QTc, signs of hypertrophic cardiomyopathy, or Brugada's Syndrome.

4.) Diaphoresis unexplained by ambient temperature, unexplained general weakness, or unexplained nausea and vomiting. Be especially suspecious if your patient is a diabetic.

5.) Suspected diabetic ketoacidosis (which may be an atypical presentation of ACS).

6.) A feeling of impending doom – Often a patient just knows something is frightfully wrong! Usually accompanied by diaphoresis unexplained by ambient temperature.

7.) Any suspected drug overdose or metabolic derangement. Be especially alert for dialysis patients who present with general weakness and/or shortness of breath!

8.) An unconscious patient (excluding cardiac arrest). On the other hand, it's one of the first things you want to accomplish when your patient experiences ROSC.

9.) Palpitations – Defined as any uncomfortable awareness of your own heart beat. Includes "skipped" beats and "racing" heart.

10.) Any heart rate less than 50 or greater than 150.

Posted by on January 20, 2009 • Filed under: ems-topics • Tagged: , ,

Differential diagnosis of wide complex tachycardias – Part VI

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Let’s take a look at a couple of rhythms you never want to see on the monitor.

First, from ABC of clinical electrocardiography – Broad complex tachycardia Part II, BMJ 2002; 324:776-779:


This is an irregular and polymorphic wide complex tachycardia that appears to show a streamer effect, or “turning of the points.”

Is it Torsades de Pointes?

The answer is, it’s impossible to tell from this rhythm strip!

Why?

Because the key distinction between polymorphic VT and Torsades de Pointes (which is a form of polymorphic VT) is that Torsades de Pointes will have a prolonged QT interval in the underlying rhythm!

This rhythm strip doesn’t show the underlying rhythm, so it’s impossible to diagnose as Torsades de Pointes, unless you can derive something useful from the history that would make you reach for the magnesium sulfate instead of the amiodarone (or defibrillator).

Since a normal QT interval varies with heart rate, what we’re really talking about is a prolonged QTc interval (the small ‘c’ stands for ‘corrected’ and normalizes the QT interval for the heart rate).

Most of the books I’ve read suggest that a QTc > 460 ms is prolonged and > 500 ms is clinically significant.

Dr. Wes has an interesting case of Torsades de Pointes here.

There are some very interesting YouTube videos that show Torsades de Pointes here and here.

Here’s another from ABC of clinical electrocardiography – Junctional tachycardias, BMJ 2002; 324:662-665:

This is an irregular and slightly polymorphic wide complex tachycardia. It’s also very fast! Anytime a tachycardia approaches 250 beats/min., you should be very suspicious of an accessory pathway (or Wolff-Parkinson-White Syndrome).

What else makes this rhythm different from the first? All of the “points” of the QRS complexes are pointing the same direction (in this case down). Familiarize yourself with this rhythm! These patients are rare, but they’re out there!

If you have atrial fibrillation on the monitor, and the shortest R-R interval is 6 small blocks or less, then you should treat it like WPW, and stay away from antiarrhythmics!

Atrial fibrillation in the presence of WPW is a very dangerous rhythm, and one of those occasions where you can kill your patient by selecting the wrong medication. The only safe drug for AF/WPW may be procainamide.

Consider this interesting transcript from Amal Mattu M.D.’s December 2008 podcast at EMedHome.com (thanks for the tip, Maciek!):

Another concern that you need to be aware of is, if you have a patient who has AF with WPW, stay away from amiodarone. Even now, AHA continues to list amiodarone as a viable option, but it’s not a viable option. In fact, the only published reports on using amiodarone in rapid AF and WPW have indicated that amiodarone is associated with adverse outcomes. There’s a handful of case reports of patients that had rapid AF and WPW. They got amiodarone and they decompensated. There are, to my knowledge – and I’ve looked through the literature in detail multiple times – and I have yet to find even a single case report or a single case series or a published study saying, “I had a patient with rapid AF and WPW, I gave him amiodarone, and they did well.” Not a single publication that I can find. The only publications on that particular scenario that have ever been published in the literature are “patient did worse” so my recommendation and a handful of other peoples’ recommendations also; “Stay away from amiodarone if you’re taking care of a patient with rapid AF and WPW.”

Remember the first rule of medicine!

If your patient is hemodynamically stable, then transport the patient to the emergency department for cardioversion. It’s probably the safest option.

You can see an example of what I’m talking about here and here.

Do you noticed any similarities between these two case studies? Look carefully!

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 16, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , ,

Differential diagnosis of wide complex tachycardias – Part V

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Let’s switch gears a little bit and discuss irregular or polymorphic wide complex tachycardias.

First I need to tell you a story.

A few years ago I was teaching ACLS to a group of mostly nurses at the local community hospital. I volunteered to teach Bradycardias, Tachycardias, and the Hypotension/Shock/Acute Pulmonary Edema algorithm.

At first the education coordinator was thrilled! Apparently not many ACLS instructors feel comfortable teaching the Hypotension/Shock/Acute Pulmonary Edema alogrithm.

Keep in mind, I was following along with the AHA ACLS PowerPoint slide set. I wasn’t freelancing. I was explaining and elaborating, but I wasn’t introducing material that is outside the scope of the ACLS objectives.

I arrived at Irregular (or Polymorphic) Wide Complex Tachycardias.

I had just written on the board the differential diagnosis, which included:

  • Atrial fibrillation/flutter or (multifocal atrial tachycardia) with bundle branch block
  • Polymorphic VT
  • Torsades de Pointes
  • Atrial fibrillation with Wolff-Parkinson-White Syndrome (WPW)

When suddenly, the education coordinator yelled out from the side of the room, “You’re scaring the hell out of them!”

I was struck dumb!

I didn’t know what to say. I looked back at the screen, and I looked at the dry erase board where I had just written the differential diagnosis, and then I looked back at the education coordinator, shrugged my shoulders, and said, “What do you want me to do?”

To be honest, this wasn’t the first run-in I had had with this particular education coordinator.

A couple of years prior, I was a student in one of her ACLS classes. She handed out a cardiac rhythm strip test. I identified one of the heart rhythms on the test as 2:1 atrial tachycardia. She marked it wrong. When I asked about it, she said the correct answer was sinus tachycardia with 2°AVB and 2:1 conduction.

I laughed and said, “Is the atrial rate > 100?”

She said yes.

“And you agree there is 2:1 conduction?”

She agreed that there was.

“So you acknowledge that 2:1 atrial tachycardia is technically correct?”

She gave me look of utter contempt, leaned forward, and said quietly, “What do you think you are? A cardiologist?”

I’m not entirely sure this person likes firefighters. Let’s just say she used to be married to one, and leave it at that.

All of this to say, the differential diagnosis of irregular (or polymorhpic) wide complex tachycardias is a very neglected subject, both in paramedic school, and in ACLS class! But you have to know the differential diagnosis to select the correct treatment modality!

You can kill a patient who presents with an irregular (or polymorphic) wide complex tachycardia if you select the wrong drug!

That should “scare the hell out of you” far more than the differential diagnosis written out on a dry erase board.

Let’s start with atrial fibrillation.

Atrial fibrillation with intraventricular conduction defect (including right and left bundle branch block) can be considered a VT mimic at high rates, because the higher the heart rate, the more difficult it is to pick up on the irregularity that is normally the hallmark of atrial fibrillation!

In training (using the heart rhythm simulator) I sometimes give paramedics a scenario like this:

89 year old female contacts 9-1-1 complaining of chest pain and shortness of breath

On arrival, respirations are 36 and labored

Skin is pale and diaphoretic

Begin your assessment!

When they attach the monitor, they see atrial fibrillation with a nonspecific intraventricular conduction defect at a rate of 160.

I take that back. What they see when they attach the monitor is a wide complex tachycardia.

This example from Wide Complex Tachycardia: ECG Differential Diagnosis. Am J Emerg Med 1999; 17:376-381 should give you an idea what it looked like when printed out (which is different from how it looks on the monitor).


When they assess the BP (if they assess the BP) it comes back 160/110.

When they asses breath sounds (if they assess breath sounds) I say “wheezes with a poor tidal volume”.

When they assess the SpO2 (if they assess the SpO2) I say “72″.

Can you guess what’s wrong with this patient?

If you said “heart failure” move to the head of the class!

You would be frightened amazed to know how many paramedics immediately lie the patient flat and prepare her for immediate synchronized cardioversion!

In the debriefing that follows, when I ask why the decision was made to start shocking the patient, the ones that have clear rationale will say, “Because she was in unstable VT!” or “Because she was in unstable AF with RVR”.

When I asked what made the patient unstable, they will say, “the chest pain!” Some will say “the shortness of breath!”

Others will want to say the BP, but then they realize they never assessed it.

There’s a fine line between symptomatic and hemodynamically unstable.

For any patient who presents with a tachycardia, one of the most important and difficult questions you have to answer is:

Is the tachycardia causing the signs and symptoms, or are the signs and symptoms causing the tachycardia?

To put it another way:

Is this some type of compensatory tachycardia?

For the heart failure patient, atrial fibrillation and bundle branch block are extremely common. Have you ever seen acute, decompensated heart failure patient that did not present with tachycardia?

This is just my opinion, but I would try oxygen (CPAP if possible) and nitroglycerin before lying a heart failure patient flat and proceeding directly to synchronized cardioversion.

The next question you need to answer is:

Does the risk/benefit analysis favor treating this tachycardia in the field?

Choose wisely!

If you read the AHA ECC 2005 guidelines, you will see this statement featured prominently in the irregular (or polymorphic) wide complex tachycardia section.

“We recommend a 12-lead ECG and expert consultation if the patient is stable.”

Was the patient in this example “stable”? No!

Was the instability cased by the atrial fibrillation and rapid ventricular response?

In my opinion, no.

The BP of 160/110 gives you “room to play” so to speak. Nitroglycerin is a potent vasodilator. Why not give it, along with supplemental oxygen, and take some preload off the heart?

The heart rate will probably come down on its own when the SpO2 is back > 90.

You can always simultaneously prepare for cardioversion!

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 12, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , ,

Differential diagnosis of wide complex tachycardias – Part IV

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Let’s look at a more typical case of wide complex tachycardia.

This case comes from Lt. Jason Kinley of Xenia Fire Division. If you’re not familiar with Xenia Fire Division in Xenia, OH, they have an outstanding prehospital 12 lead ECG program. Jason is also one of the co-moderators at the EMS-to-Balloon (E2B) Challenge! listserv at Yahoo!

Here’s the story.

EMS is called for a 89 year old male with chest pain. Onset 30 minutes ago. Non-radiating. Patient is A+OX4. Skin is moist. Skin color is good. No increase in respiratory effort. Meds for diabetes, hypertension, and unspecified heart problem (patient is a poor historian). The patient is reluctant to go to the hospital. He states he was seen 4 days ago for a possible TIA.



Yes, I know the computerized interpretive statement has been removed. That’s my fault!

Here are the computer measurements:

HR: 150
PR: *
QRS: 126
QT/QTc: 304/475
P-R-T: * -51 110

The treating paramedics correctly identified this as a regular wide complex tachycardia. Because the patient was hemodynamically stable, they initiated a 150 mg bolus of Amiodarone over 10 minutes, with no change to the heart rhythm.

Why Amiodarone?

Because according to the 2005 AHA ECC guidelines, that’s the drug you give for undifferentiated regular wide complex tachycardia. It’s supposed to be therapeutic for both ventricular and supraventricular tachycardias.

You will remember the patient stated that he was seen 4 days prior for a possible TIA. Well, it turns out that the same EMS system brought him to the hospital. As luck would have it, they performed a prehospital 12 lead ECG at that time.

Here it is.


Computer measurements:

HR: 100
PR: 232
QRS: 134
QT/QTc: 350/451
P-R-T: 50 -56 91

Now compare the QRS morphology in the first PH12ECG to the PH12ECG taken 4 days prior, when the patient was in borderline sinus tachycardia with 1°AVB.*

Is it a match? You bet! This patient has a pre-existing intraventricular conduction defect (or atypical LBBB). Note the S wave in lead V6.

Was this patient in ventricular tachycardia? No.

Considering the heart rate of exactly 150, the pseudo-R wave in lead V1 during the tachycardia, and the recently history of possible TIA, 2:1 atrial flutter is the most likely explanation.

However, the first rule applies! In the absence of an “old” ECG for comparison, it’s VT until proven otherwise.

The patient didn’t covert to sinus rhythm, but it was a well-executed call, and no harm came to the patient.

* 3:1 atrial flutter is also a possibility. Note the heart rate of exactly 100.

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 9, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , ,

Differential diagnosis of wide complex tachycardias – Part III

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Let’s look at another unusual case.

This was the ECG of a chest pain patient in the emergency department.


Let us assume for a moment that the patient is hemodynamically stable but diaphoretic and complaining of severe substernal chest pressure.

What does this 12 lead ECG show?

It’s a regular rhythm. The rate is 120. The QRS duration is 150 ms (0.15 s). This is a regular wide complex tachycardia.

No P waves are apparent. Could this be slow VT?

Let’s look at QRS morphology.

The pattern in lead V1 is RBBB and there is a left axis deviation. This is a bifascicular pattern (RBBB/LAFB).

Suddenly, there is a rhythm change on the monitor.

What happened?

Atrial complexes can be seen in several leads at a rate very similar to the rate of the wide complex tachycardia.

This was some type of SVT with bifascicular block.

The PR interval was sufficiently long that it was buried in the previous T wave, making this a “trifascicular” block (1°AVB, RBBB, LAFB).

Think about it. If the right bundle branch is blocked, and the left anterior fascicle of the left bundle branch is blocked, then ventricular activation occurs only through the left posterior fascicle of the left bundle branch.

When 1°AVB occurs in this setting, there’s either a delay in the AV node, or a delay in the left posterior fascicle of the left bundle branch. Either way, with a chest pain patient (or a syncope patient) you have to be concerned that the last remaining connection between the atria and ventricles is vulnerable.

These patients can suddenly convert to 3°AVB without an escape rhythm, especially if they take oral antiarrhythmics.

So be careful when considering IV antiarrhythmics for these patients, and consider applying the Combo-Pads as a precaution.

The 2005 AHA ECC Guidelines frown upon TCP for asystolic arrest, but in the setting of bifascicular block and chest pain (or a recent history of syncope), it seems to me* that immediate TCP is a reasonable intervention if the Combo-Pads are already applied as a precaution in anticipation of the possibility!

Just remember, this would not be the time to get shy about dialing up the milliamperes!

Besides, you know how it goes! If you prepare the patient with Combo-Pads, you won’t need them! :)

* I’m not your Medical Control Physician, so please don’t sue me. This is just my opinion.

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 3, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , ,

Differential diagnosis of wide complex tachycardias – Part II

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By definition, a wide complex tachycardia is a heart rhythm with a QRS duration ≥ 120 ms (0.12 s) and a ventricular rate ≥ 100.

When this criteria is met, and the the rhythm is regular (no variability in the R-R interval) then it’s a regular wide complex tachycardia.

This is a very broad and inclusive definition of regular wide complex tachycardia! But in my experience, it’s the best way to approach the problem. It keeps you out of trouble!

The differential diagnosis for regular wide complex tachycardia includes:

  • SVT with BBB or aberrancy (includes sinus tachycardia and atrial flutter)
  • Ventricular tachycardia
  • Paced rhythms
  • Atrioventricular reentrant tachyardia (AVRT) with antidromic conduction (WPW)
  • Electrolyte derangement or drug toxicity

Take a look at the following ECG which was recorded from a postictal seizure patient.

Using the large block method, we know the ventricular rate is > 100 and the QRS duration is > 3 small blocks, or 120 ms (0.12 s).

The rhythm is regular, so this is a regular wide complex tachycardia.

The next question we need to ask is, “Could this be VT?”

For this ECG, the computer measured the heart rate at 119, which makes VT unlikely, but still a possibility.

This tachycardia also shows LBBB morphology with a left axis deviation. This is the expected pattern for a paced rhythm with the pacing lead in the apex of the right ventricle, so that also needs to be considered.

There are two things you can do to rule this out. The first is to simply expose the patient’s chest and look for a pacemaker pocket. The second is to look for the telltale “blips” in front of the QRS complexes.

Sometimes this is only visible in one lead, so look carefully!

Next, we should look for sinus P waves. A ventricular rate of 119 suggests sinus tachycardia. Sinus tachycardia must be part of the differential diagnosis for regular wide complex tachycardias!

Do you see any P waves? Look at the downslope of the T waves in the inferior leads (I, II and III) and lead V2. There’s some type of atrial complex there, and it could be a sinus P wave. Or, this could be an atypical 2:1 atrial flutter (atrial flutter with an abnormally slow flutter rate).

Either way, there appears to be a clear relationship between P waves and QRS complexes, suggesting a supraventricular origin.

Let’s look at another case.

This ECG was recorded on an interfacility transport with a patient experiencing an intracranial hemmorhage.

Here we have a regular wide complex tachycardia with a left axis deviation. Whenever I see a rhythm strip showing a wide complex tachycardia with a right or left axis deviation, I try to guess whether or not the QRS complex will be positive or negative in lead V1.

If it’s positive, then it will be a bifascicular pattern. If it’s negative, then it will be a LBBB with left axis deviation, which is the expected pattern for a paced rhythm when the pacing lead is in the apex of the right ventricle.

Does this patient have a pacemaker? Yes!

If you look at the bottom of this ECG, the block arrows are the LP12′s pacing detector. They’re not always accurate, but it increases the possibility that this is a paced rhythm.

The paramedic in charge of the transport elected to perform a 12 lead ECG.

This 12 lead ECG shows LBBB morphology (rS complex in lead V1 and a monophasic R wave in lead I).

If you look carefully at this 12 lead ECG, you can see little “blips” in front of the QRS complex in leads V3-V6. They also line up with the block arrows from the pacing detector.

This is a paced rhythm.

Is the pacemaker functioning properly? Who knows! You’d have to understand how the pacemaker is programmed to answer that question. In the meantime, a paced rhythm at 125 ppm probably isn’t hurting the patient, and required no intervention during the transport.

The other thing you might notice about this ECG is that the GE-Marquette 12SL interpretive algorithm is giving the ***ACUTE MI SUSPECTED*** message.

Why?

Probably because of the discordant ST segment elevation > 5 mm in several leads and the concordant ST segment depression in lead V2.

Just remember, neurological insult can create ST changes similar to STEMI on the 12 lead ECG! Patients who present with an abnormal neuro exam and an ECG suggestive of STEMI generally get a CT scan before they are sent to the cath lab.

Is this a STEMI? Probably not.

Next time, we’ll look at another unusual presentation of a regular wide complex tachycardia with an unexpected outcome!

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 1, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , ,