Narrow complex tachycardias - Part II

Here's a call that was very well executed.

The patient was a 35 year old Hispanic female; walk-in patient at a volunteer clinic.

Through an interpreter it was learned that the patient was complaining of palpitations and slight chest discomfort.

The onset was sudden.

The medical history was significant for "arrhythmias".

No medications.

Skin: warm and dry with pink oral mucosa

Vital signs were assessed.

Resp: 20
Pulse: Too rapid to count
BP: 104/58
SpO2: 97 on RA

The cardiac monitor was attached.

A 12 lead ECG is captured.


Here is the rhythm strip.


It is very important to document cardiac arrhythmias in 12 leads whenever possible.

Once the arrhythmia resolves (on its own or with our help) the opportunity to document the arrhythmia is gone.

The 12 lead ECG can be invaluable to the cardiologist/electrophysiologist who follows up on the patient!

It can also be invaluable to YOU when you're trying to figure out what you're dealing with.

The patient was placed on oxygen.

An IV was started and labs were drawn.

The paramedic in charge of the call reviewed the Hs and Ts and found no evidence that it was a compensatory tachycardia.

6 mg adenosine was given rapid IV push followed by a 20 ml bolus of 0.9% NS.

The paramedic remembered to press the PRINT button prior to giving the drug.

The following two rhythm strips are continuous.


Sinus rhythm was restored and the patient reported relief of her symptoms.

As a side note, I like to show these rhythm strips to new paramedics and ask them to interpret the heart rhythm. :)

Since the monitor was already attached, it was a simple matter to capture a post-conversion 12 lead ECG.


The patient was transported to the emergency department and the paramedic was able to provide excellent documentation of the prehospital interventions, with outstanding data quality.

Narrow complex tachycardias - Part I

I've come to dislike the term "SVT" (supraventricular tachycardia).

In the first place, it's not an arrhythmia. It's an umbrella term that covers a group of arrhythmias which require the AV node for their maintenance.

Most importantly, it includes sinus tachycardia!

For some reason, this is a difficult concept for many clinicians to grasp, partly because of myths passed on from generation to generation.

For example, my least favorite of all.

"If the rate is 150 or greater, it's SVT."

Forgive me, but what in the Wide World of Sports is that supposed to mean?

Does it mean that junctional tachycardia at a rate of 149 is not SVT?

I think the term "SVT" is less helpful than the term "narrow complex tachycardia" for figuring out a differential diagnosis.

Why?

Because at first glance, you won't always know it's SVT, but you should be able to figure out whether or not a tachycardia has narrow QRS complexes.

Regardless, there's no point in wasting precious time and energy making this more difficult than it needs to be.

A tachycardia is a heart rate equal to or greater than 100. A supraventricular rhythm originates above the ventricles. A narrow QRS rhythm has a QRS duration < 120 ms.

From the AHA ECC 2005 Guidelines, Part 7.3: Management of Symptomatic Bradycardia and Tachycardia:

Narrow–QRS-complex (SVT) tachycardias (QRS duration < 0.12 s) in order of frequency

• Sinus tachycardia
• Atrial fibrillation
• Atrial flutter
• AV nodal reentry
• Accessory pathway–mediated tachycardia
• Atrial tachycardia (ectopic and reentrant)
• Multifocal atrial tachycardia (MAT)
• Junctional tachycardia
  

In other words:

Sinus tachcyardia is, by far, the most common form of SVT!

This is important because the first arrhythmia you should consider when faced with a narrow complex tachycardia (or SVT) is sinus tachycardia!

And what antiarrhythmic do we use for sinus tachycardia?

All together now!

NONE!

We consider the Hs and Ts (as we should for any arrhythmia before reaching into the drug box) and we treat the underlying cause.

Let me give you an example.

An 18 year old female calls 9-1-1 and complains of palpitations.

EMS responds to the scene and finds her lying on the floor with absent radial pulses and a pressure of 80/40.

However, she's conscious, alert, and oriented to person, place and time.

The cardiac monitor is attached.


The paramedic in charge of the call diagnosed the heart rhythm as SVT.

An IV was started, and the patient received adenosine 6/12/12.

It didn't resolve the arrhythmia.

Why?

Because had they asked, the patient had an elective abortion earlier that day.

She had vaginal bleeding and soaked through at least 8 maxipads.

In light of this new information, what is the heart rhythm?

How about sinus tachcyardia?

How about appropriate and compensatory sinus tachycardia?

So what was the patient's problem? If you don't know, it's on this list and it starts with an H.


Do you see why it's important to include sinus tachycardia in the differential diagnosis for tachycardias?

Failure to consider sinus tachycardia can have serious consequences and put the patient at risk for iatrogenic harm.

See also:

Narrow complex tachycardias - Part II

Acute inferior STEMI - RCA or LCX?

The revelation that the LCX was the culprit artery in the recent case study made me go back to the peer reviewed literature to see where I went wrong.

Let's look at the evidence.

From Sgarbossa et al., Electrocardiographic diagnosis of acute myocardial infarction: Current concepts for the clinician. Am Heart J. 2001;141:507-17:

"The typical electrocardiographic pattern of inferior infarction consists of ST-segment elevation in leads II, III, and aVF. The occlusion is in the RCA in 80% to 90% of cases and is in the LCX in the remaining patients. Higher ST elevation in lead III than in lead II strongly suggests compromise of the RCA.

A bedside differential diagnosis between culprit arteries can also be attempted by examining additional electrocardiographic leads. Because the only lead that faces the superior part of the left ventricle and directly opposes the inferior wall is aVL, ST depression in lead aVL is almost always determined by RCA occlusion (sensitivity, 94%; specificity, 71%), without indicating concomitant involvement of the posterior wall or the right ventricle. Injury in leads II, III, and aVF without ST depression in aVL indicates proximal LCX occlusion.

Several studies in the 1980s concluded that ST elevation in leads V5 through V6 during inferior injury signaled LCX occlusion. However, because most inferior infarctions are caused by RCA occlusion, the positive predictive value of this sign is poor. The arteries that supply the posterolateral region of the left ventricle are the obtuse marginal branch of the LCX, the posterolateral, and the LAD branches. Thus ST changes in leads V5 and V6 indicate rather posterolateral ischemia triggered by either RCA or LCX occlusion. When this ST elevation is significant (>2 mm), it is probably a sign of "mega-artery-related" (either the RCA or LCX) infarction with a large ischemic burden."

Let's look at the 12 lead ECG from the case study:


ST elevation in leads II, III and aVF? Check.

ST elevation lead III > ST elevation lead II?


Close. A virtual tie. (Note that I'm measuring the ST elevation from the TP segment to the J point). There may be slight advantage to lead III with calipers.

Remember this table from Eskola et al. How to Use ECG for Decision Support in the Catheterization Laboratory - Cases With Inferior ST Elevation Myocardial Infarction. Journal of Electrocardiography Vol 37 No. 4 October 2004?


It states that when ST elevation in lead II is equal to ST elevation in lead III, you should consider the T wave amplitude!

Well, that's no help either, since the T wave amplitude in leads II and III are also the same.

Moving on...

ST depression in lead aVL? Check.

ST elevation in leads V5 and V6? Less than 2 mm, but check.

If you had to venture a guess based on these criteria, the smart money would be on the RCA.

Now let's look at modified leads V4R and V5R.


This created some cognitive dissonance for me. I was surprised not to see ST elevation in these leads, particularly with the clinical correlation of borderline bradycardia and hypotension.

Let's look at our cheat sheet.


We're forced to say that lead V4R is inconclusive in this case because the ST segment and T wave are both isoelectric, which supports neither the RCA or the LCX.

In the last analysis, you can't always identify the culprit artery based on the 12 lead ECG (or in this case, the 14 lead ECG).

Either that, or you have to be smarter than I am (in which case you should leave a comment).

This patient's unusual coronary anatomy (I'm tempted to call it a mega-LCX) seems to confound the commonly accepted criteria.

It's still fun to guess! :)

I've often said that acute inferior STEMI should be treated as RV infarction until proven otherwise!

I still feel that way. It's interesting that leads V4R and V5R correctly identified that the patient was not experiencing RV infarction, but with the hypotension, the patient still required a fluid bolus.

Was it worth the paramedic's time collecting leads V4R and V5R?

I'm not sure it changed anything for the patient, but it is interesting from an academic perspective!

62 yom CC: chest discomfort (update)

I was wrong.

There, I said it.

Someone please let my girlfriend know.

The culprit artery for the 62 yom c/o chest discomfort was the LCX, not the RCA as I suspected.

I'm trying to figure out how to load the DICOM images into a format viewable on my blog (so you can see the live-action angiograms).

In the meantime, here are the still images. Discussion to follow.

Before - proximal occlusion of the LCX

Before - Proximal occlusion of the LCX

After - Note how the distal LCX branches off and supplies the inferior wall

After - Note how the distal LCX branches off and supplies the inferior wall

Very small and non-dominant RCA

Water Spouts

Yesterday morning as I was getting off duty, dispatch contacted the fire station to let us know that up to 3 water spouts had been reported in the area.

I love water spouts, and I've been waiting 12 years (the time I've lived on Hilton Head Island) to see one in real life!

It turns out there was a water spout just off the coast along South Forest Beach. I could have turned left out of the fire station, driven one block, and watched it for 15 minutes!

Maybe next time. On the plus side, a lot of people saw the water spouts and took pictures, which can be viewed at the Island Packet's website.

Image credit: Brian Vaughn, www.islandpacket.com

Image credit: Jeff Davidson, www.islandpacket.com

See the rest of the photos HERE.

Why 12-leads?

If for no other reason, because MONA can "clean up" a 12 lead ECG, making it non-diagnostic by arrival at the hospital!

Before MONA


After MONA


If not for the prehospital 12 lead ECG, there's no telling how long this patient would have lingered in the emergency department!

*** Update ***

Here's another case (from several years ago) that helps illustrate the point.

This was from a chest pain patient who was transported to my jurisdiction from a neighboring EMS system by boat.

Image credit: Wikipedia (Jeff Morgan www.findparadise.com)

In other words, it was an EMS transfer. We met them at the dock and took the patient to the hospital.

Here is the ECG that was handed to me by the transferring paramedic (who recognized it was showing acute inferior STEMI).

I'm pretty sure it was recorded by a LP11.


You'll notice that part of the computerized interpretation came off when I peeled back the scotch tape.

Here is the 12 lead ECG I captured en route to the hospital (using the exact same electrodes).


The ECG had become nondiagnostic.*

I'd love to tell you that the (first) prehospital 12 lead ECG saved the day. It didn't. I personally showed it to the ED physician, but he was dismissive. No urgent action was taken.

I have no idea what ended up happening to the patient.

* Note: You can still identify acute inferior STEMI in the second ECG by the Q waves and non-concave ST segments in leads III and aVF, along with the downsloping ST segment in lead aVL. However, it's the first prehospital 12 lead ECG that really tells the tale!

62 yom CC: chest discomfort

EMS is dispatched to a 62 year old male with a chief complaint of chest discomfort. On arrival, the patient is found sitting at the dinner table. He appears acutely ill.

Onset: Fairly sudden after sitting down for dinner 20-30 minutes ago
Provoke: Nothing makes the pain feel better or worse
Quality: Dull pressure/ache
Radiation: The pain does not radiate
Severity: 8/10 "feels like a 747 is sitting on his chest"
Time: Feels slightly better since the onset

Skin: cool, pale, diaphoretic

Vital signs:

Resp: 20
Pulse: 62
BP: 84/48
SpO2: 99 on RA

Breath sounds: clear

The cardiac monitor is attached.



A 12 lead ECG is captured.


The paramedic trouble-shoots the loose electrode. The data quality looks good to me, but the computer disagrees!


Three's a charm!


Now what? You're 5 minutes into the call...

*** Update ***

The paramedic in charge of the call elected to perform an additional 12 lead ECG using modified leads V4R and V5R.

Here is the result.


Here are some charts from my series on right ventricular infarction for reference. I don't remember where the first chart came from, but it shows the ramifications of various ST/T configurations in lead V4R.


Also consider Eskola et al. How to Use ECG for Decision Support in the Catheterization Laboratory - Cases With Inferior ST Elevation Myocardial Infarction. Journal of Electrocardiography Vol 37 No. 4 October 2004.


Question: Does this change anything? Why or why not?

See the update, including angiograms HERE.

35 yom CC: palpitations

35 year old male (on vacation) presents to the fire station complaining of an irregular heart beat.

History of present illness: Patient states he walked up to the top of the lighthouse earlier in the day and started to feel palpitations.

PMH: Healthy
Meds: None

Vital signs are assessed.

Resp: 18
Pulse: 54 (irregular)
BP: 130/84
SpO2: 99 RA

The cardiac monitor is attached.

A 12 lead ECG is captured.


The patient is adamant that he does not want to be transported to the hospital. He states that he just wants a printout of the 12 lead ECG to show his private physician.

What is your interpretation of this ECG?

How would you explain to this patient the risk of refusing care/transport?

Right bundle branch block - Part III

Let's take another look at the ECG from Part II.


I asked you to look carefully at this ECG, and then using the concept of appropriate T-wave discordance, see if anything bothers you.

Does anything stand out?

How about lead V4?


Here you can see the terminal deflection (blue arrow) is positive, and so is the T-wave (inappropriate T-wave concordance). There is also at least 1 mm of ST segment elevation. That's definitely abnormal!

Now let's look in the inferior leads. They all look abnormal, but I'm going to use lead aVF as the example.


The terminal deflection is negative (blue arrow) and the T wave is also negative (inappropriately concordant T-wave). The inferior leads are reciprocal to the anterior leads. Could this represent reciprocal changes? Absolutely!

It is sometimes said that reciprocal changes are of no value in the presence of bundle branch blocks. That's not entirely true! You just have to interpret them within the context of appropriate T-wave discordance.

In other words, in the presence of bundle branch block, if the terminal deflection of the QRS complex is negative in lead III and positive in lead aVL, then you will have pseudo reciprocal changes (positive in lead III and negative in lead aVL). This is a normal finding in left bundle branch block, for example.

If, however, the terminal deflection of the QRS complex is negative in lead III (as in this ECG) and the same lead is showing inappropriately concordant ST-segment depression or T-wave inversion, then it's probably not a pseudo reciprocal change. Why? Because it's opposite the expected pattern.

I'd also like to point out that leads V2 and V3 look really strange in this ECG. Why? Because there's a merging together of the S-wave and T-wave (sometimes seen in severe hyperkalemia). This is a really ugly T-wave abnormality, especially since we would normally expect a terminal R wave in lead V2 with right bundle branch block.

Something's going on here!

Let's look at some serial ECGs. This one was taken just 4 minutes later.


Now what do you see?

*** Update 07/13/09 ***

Here's the final ECG in the series, recorded as the ambulance arrived at the hospital.


Quite a difference! Once again, it's easy to see the value of serial ECGs.

Let's take a look at lead V2 and see how it changed from the first ECG to the last.


The problem (or perhaps the challenge) is that this final piece of the puzzle wasn't present until arrival at the hospital. Fortunately, it was one of 17 PCI hospitals in the State of South Carolina!

This is why paramedics need to be able to interpret a 12 lead ECG at a high level. Every Patient Counts! We need to make sure that STEMI patients are delivered to the right hospital!

QRS confounders like right and left bundle branch block can make the ECG diagnosis of STEMI more difficult, but these are the patients who receive the most benefit from reperfusion therapy, and prompt, expertly performed primary PCI is the preferred strategy!

We shouldn't delay a high risk patient's care because we can't read their ECG. Unfortunately, it happens every day all over the country.

That's assuming the EMS system has 12 lead ECG monitors in the first place.

See also:

Right bundle branch block - Part I

Right bundle branch block - Part II

82 yom CC: chest pain

"Funky Troubling Looking" -- Right Bundle Branch Block and MI

Right bundle branch block - Part II

Once you've identified a RBBB on the 12 lead ECG, the next thing you want to do is determine whether or not you're dealing with a normal RBBB or an abnormal RBBB (or new RBBB).

You may remember this graph from my previous post: Who benefits the most from reperfusion therapy?


It shows that patients with "new BBB" receive the most benefit in terms of lives saved per 1000 treated with fibrinolytics (based on the FTT Collaborate Group). We often here it claimed that patients with "new LBBB" receive the highest benefit from prompt reperfusion therapy, but it's worth pointing out that the FTT Collaborative Group did not distinguish between LBBB and RBBB.

Generally speaking, RBBB does not mimic or obscure the ECG diagnosis of acute STEMI the way LBBB does. However, sometimes it can (remember the update to Funky Trouble-Looking RBBB with AMI).

So how do we know what's "normal" for right bundle branch block? We use the concept of "appropriate T wave discordance". This concept usually comes up in the context of discussing LBBB, but it's also useful for RBBB (and paced rhythms, ventricular rhythms, non-specific IVCD, and so on).

For RBBB, the concept is that when the terminal deflection of the QRS complex is positive, the T wave should be negative. Likewise, when the terminal deflection is negative, the T wave should be positive.

You may recall this graph from my previous post: Identifying AMI in the presence of LBBB - Sgarbossa's Criteria - Part II.


The blue and red arrows show the expected relationship between the terminal deflection and the T wave with RBBB.

Remember, the terminal deflection is the last deflection in the QRS complex.

Consider the following case.

EMS is contacted for a 77 year old male complaining of chest pain. On arrival, you find the patient lying supine on the couch. He is ashen in color and diaphoretic with absent radial pulses. He responds sluggishly but appropriately and states that he is having severe sub-sternal chest pain.

His shirt is cut off and the combo-pads are applied, revealing the following heart rhythm.


It appears to be sinus rhythm with wide QRS complexes and occasional PVCs.

A 12 lead ECG is captured.


Using the concept of "appropriate T wave discordance" is there anything about this ECG that bothers you?

See also:

Right bundle branch block - Part I

Right bundle branch block - Part III

Happy 4th of July weekend

Sorry I haven't posted anything in a while, but I've been away at my parents beautiful log home on Lake Huron. It's been nice to get away for a while and enjoy some crisp northern air!

I've been power washing, painting, and digging all week (the artesian well sprang a leak -- who knew trench rescue would have real-world applications?)

Here is a video I shot the other morning with my Canon PowerShot A450 (cheap little point and shoot camera I purchased at Walmart that takes surprisingly good video).


The sun finally came out yesterday!

I may add more photos later tonight. I hope you're having a great 4th of July weekend!

Be safe. See you soon!

*** Update 07/10/09 ***

Restoration of the "bear tree"

Before


After