81 yof CC: ICD shocks x6

EMS responds to a 81 year old female who was implanted with "a pacemaker" 2 weeks ago. She complains that the device has shocked her 6 times.

On arrival the patient is found sitting in a chair. She is anxious but alert and oriented to person, place, time and event.

Vital signs:

Resp: 18
Pulse: 164 and irregular
BP: 128/68
SpO2: 98 on RA

The patient is asked if she carries an ID card for her implantable device and she finds this card in her purse.


A 12 lead ECG is captured (I am using the 12-lead that shows the best data quality which was taken en route to the hospital).


Here is a typical looking rhythm strip during the transport.


Why do you think this patient's ICD is firing?

What would you do about it?

Found on the Lifenet Receiving Station

Is there anything about this ECG (other than the poor data quality) that interests you?

The patient was a 90 year old male, fall with injury. Also complaining of pain between the shoulder blades.

*** Update 11/08/09 ***

This ECG caught my eye because it satisfies one of Sgarbossa's criteria for the identification of AMI in the presence of LBBB. Specifically, the concordant ST-segment depression in lead V3 is a highly suspicious finding.

I give a fairly extensive review of Sgarbossa's criteria here:

Identifying AMI in the presence of LBBB - Sgarbossa's Criteria - Part I
Identifying AMI in the presence of LBBB - Sgarbossa's Criteria - Part II


As a stand-alone finding, concordant ST-segment depression in a right precordial lead gives this ECG a score of 3 out of 10 (probability of AMI 66%).

I personally don't think it's necessary to score the ECG. As far as I'm concerned, an ECG that meets any of the criteria should be considered equivalent to an ECG showing acute STEMI, especially when you consider the depth of the S-wave in leads showing discordant ST-elevation (see previous posts on this issue).

So was this patient experiencing an acute STEMI? Here's what I found out.

Patient (90 y.o.) arrived via EMS from XXXXXXXX after falling; there was no LOC, but did complain of back pain between the shoulder blades and diffuse abdominal pain. Extensive PMH: AAA, non-operable, HTN, CAD, CABG, LBBB, anemia, cardiomyopathy and dementia. The ED physician spoke to the daughter extensively who did not want her father worked up, but did consent to a thoracic x-ray and stated she only wanted him to receive pain medication and return transport to the XXXXXXXX and did not want any further diagnostics noting that his dementia worsens when he is out of his environment. He has a living will /advanced directive on file and with him a DNR order.

He was given pain medication in the ED, the thoracic film showed no acute injury and a prescription for Lortab was written and he was sent back to the nursing home. He did not have an EKG performed on this visit or any other diagnostics. The patient was here for an admission in 6/2009 and it appears that the EKGs are very similar.

Very interesting!

When designing a STEMI program you have to make difficult choices when it comes to exclusion criteria like age, DNR status, and neurological status. Was this patient experiencing an acute thrombotic event in an epicardial coronary artery? I guess we'll never know.

It's possible this ECG finding was old and it's possible it was secondary to aortic dissection or aneurysm.

65 yof CC: Chest pain

EMS is called to a hotel for a 65 year old female complaining of chest pain.

On arrival, the patient is found sitting on the edge of the bed in her hotel room. She is alert and oriented to person, place, and time.

Her skin is pink, warm, and dry.

Onset: 30 minutes ago while getting ready for bed.
Provoke: Nothing makes the pain better or worse.
Quality: Patient states the pain is "like a vice".
Radiate: Pain radiates to the neck and left arm.
Severity: Patient gives the pain a 9/10.
Time: No previous similar episodes.

Past medical history: Thyroid disease and thyroid removal. Recent checkup at the doctor's office was unremarkable.

Medications: Unknown

The patient states that she thinks today's problem might be related to her thyroid.

Resp: 18
Pulse: 76
BP: 130/78
SpO2: 99 on RA

The cardiac monitor is attached.


A 12-lead ECG is captured.


A "clean" rhythm strip is captured.


An additional 12-lead ECG is captured in the ambulance.


This arrhythmia is documented en route to the hospital.


Your thoughts on the case?

Update to: 78 yom CC: "Chest heaviness"

Lots of interesting comments on this case.

Here is the update.

I opted to treat this patient as a presumed monomorphic ventricular tachycardia which is hemodynamically stable. I placed an 18 ga catheter in his left AC at a TKO rate. At approximately 1005 I administered 130mg (1.5mg/kg) of Lidocaine slow IV push which had no effect. At approximately 1010 the patient started vomiting profusely in a projectile fashion. He complained that he now hurt everywhere and he had a headache. At this point we decided to move to the truck even more rapidly than we already were. Enroute I gave him a second dose of Lidocaine this time 65mg (0.75mg/kg) with again no effect at approximately 1015.

At 1017 we arrived in the ER driveway and as my partner was placing the vehicle in park the patient went semi-conscious with a GCS of 9 (E3 V2 M4) and an absent radial pulse. We rapidly unloaded him to the already pre-alerted and waiting ER team. Within several minutes they successfully cardioverted the patient after one shock with a resultant bradycardic sinus arrythmia from 48-56 for a HR. He was subsequently transferred without incident to the regional tertiary care centre for ICD insertion.

Here are the serial ECGs that were captured en route to the hospital.



This case was handled very well, in my opinion. If you've read my tutorial on the differential diagnosis of wide complex tachycardias, then you know I believe that wide complex rhythms should be considered ventricular until proven otherwise!

I might not have given a second dose of lidocaine if the patient started projectile vomiting after the first dose, but it's impossible to know the proximate cause.

Here are some recent comments on the case left by a reader named Billy.

Although VT should be the default diagnosis for a wide complex tachycardia, what sort of criteria do you suggest be used other than QRS morphology?

What sort of criteria to determine that a wide QRS rhythm is supraventricular? That's an interesting question. Personally, I would require an old ECG for comparison, irregularity to suggest atrial fibrillation, the appearance of flutter waves, or a spontaneous slowing of the heart rate that reveals the rhythm to be sinus tachycardia.

What do you mean by VA conduction not being able to be differentiated from AV conduction? Are you saying that VT can produce retrograde conduction to the atria, resulting in a P wave after the QRS complex originating from the ventricles?

That's exactly what I'm saying!

Also, I didn't mean to say that because there appears to be a bifascicular block that makes it SVT. I was wondering why you thought that was unlikely in the first place for this patient, which would suggest VT.

Not to beat a dead horse, but "wide and fast" suggested VT prior to identifying the QRS morphology. VT can mimic virtually all intraventricular conduction defects! I thought RBBB/LPFB was unlikely because the RBBB morphology was atypical in lead V1 (with serial ECGs it became more typical). "Wide and fast" meant VT before we learned how to identify RBBB, LBBB, and bifascicular blocks. Unfortunately, many paramedics seem to throw that right out the window once they learn how to recognize these patterns! It's very dangerous thinking.

I am interested to how akroeze ended up treating this patient. Regardless, I think amiodorone would be a good choice. Correct me if I'm wrong, but I believe amiodorone works on many mechanisms, including Ca, K and Na channel blocking, as well as beta blocking, which makes it effective on both VT and SVT's. In these types of situations where a wide complex tachycardia might be SVT amiodorone should treat the arrhythmia no matter where the pacemaker is, making it a safe choice, whereas cardizem would be a better choice in narrow complex SVT's since its Ca channel blocking is more pronounced.

I agree with that! Amiodarone would have been a perfectly acceptable antiarrhythmic to try in this scenario. In the absence of amiodarone, lidocaine was a viable option.

I would also like to present a "chicken vs. egg" question: What if this is in fact an MI? If you use the 220-age rule then this patient's maximum heart rate is 142. With the heart rate being 180 I think it's pretty clear this patient's problem is an arrhythmia and not an MI (though we might see an MI once the arrhythmia is corrected). Suppose the patient was a bit younger and the heart rate is borderline at about 140 or so, with the same morphology in all leads. I think you can make an argument for inferior ST depression with elevation in the lateral leads. So, do you treat the tachycardia, or for ACS?

Tachycardia in the setting of acute STEMI is bad. For sinus tachycardia you treat the underlying cause. I've seen several cases of sinus tachycardia and acute STEMI mimicking a wide complex tachycardia, so you're wise to consider it. It's also not unheard of for STEMI patients to experience VT, so you could easily see an acute injury pattern coexistent with VT. All I can tell you is that no one said our job was going to be easy! Sometimes the best thing we can do for our patients is recognize our own limitations.

Left anterior fascicular block (LAFB)

A reader by the name of Jesse contacted me and wrote:

I have a question. I'm trying to learn more about fasicular and hemi blocks. I was curious if you have posted, or intend to post, any information regarding these. I understand this is all done on your free time, so no rush at all. Any helpful information that you have the time to spare will be greatly appreciated.

That sounded like a pretty good idea, so I thought I'd start with left anterior fascicular block (LAFB).

But first, we need to answer a more basic question. What is a fascicle?

Take a look at this simple diagram of the heart's electrical conduction system.

Basically what you see here is an outline of the heart. In the center is a schematic of the "cartilaginous ring" or "fibrous skeleton" of the heart. It's made of collagen (the most abundant protein in nature) and it serves several functions.

It gives structure to the heart and the AV valves in particular, so the heart doesn't collapse during systole. It's also electrically inert, so it insulates the ventricles from the atria. The only legitimate electrical connection between the atrial and ventricles is the AV node and AV bundle, which acts like a capacitor, slowing electrical impulses down and then transmitting them to the ventricles.

This slowing of the impulse through the AV node corresponds to the PR interval on the surface ECG. That's important because the delay allows time for ventricular filling. In addition, it prevents sudden death for patients that experience atrial fibrillation. When the atria are fibrillating, what's to stop the ventricles from fibrillating? The AV node!

That's exactly why accessory pathways are dangerous, especially in the presence of atrial fibrillation!

So, following the AV bundle down you can see that it bifurcates into the right and left bundle branches. The right bundle branch has one fascicle (or branch) and the left bundle branch has two fascicles (or sub-branches). They are called the left anterior fascicle and the left posterior fascicle.

The fascicles are part of the heart's electrical conduction system (the His-Purkinje system). Here's another diagram I found on the web.


You can see that the fascicles actually fan out into the ventricles to allow coordinated and synchronous ventricular activation.

Sometimes, one or more of these fascicles can become "blocked" and fail to conduct electrical impulses. Depending on where the "block" takes place, you can get a RBBB, LBBB, LAFB, LPFB, or bifascicular pattern on the 12-lead ECG.

Often the block is the result of heart disease. Sometimes, the block is secondary to an acute process like acute myocardial infarction. In fact, new bundle branch block is a disturbing finding for a STEMI patient. They derive the highest benefit from thrombolytic therapy.

Let's assume for a moment that the left anterior fascicle of the left ventricle is blocked.

What would this look like on the 12-lead ECG?

Here are the rules for interpretation of left anterior fascicular block (LAFB).



This is an example of why axis determination is an important part of 12-lead ECG interpretation. The most common causes of left axis deviation are left anterior fascicular block and inferior Q waves secondary to acute myocardial infarction.

Let's look at an actual example. The following ECGs were captured from a firefighter I used to work with. He had a known history of left anterior fascicular block (LAFB) which was apparently benign (after lots of expensive testing).

First, the rhythm strip.


Here we have a sinus rhythm with left axis deviation.

Now the 12-lead ECG.


Here we can see that the QRS duration is prolonged at 110 ms (but under 120 ms). We also note qR complexes in leads I and aVL and rS complexes in leads II, III and aVF.

It doesn't always look this perfect, but it doesn't have to. As I've said on previous occasions, our patients don't always read our textbooks!

One last feature I want you to notice is the poor R-wave progression and late transition! This is a normal finding for left anterior fascicular block (LAFB).

Next time, we'll address left posterior fascicular block (LPFB) which is a very rare isolated finding and requires a few caveants!

12-Lead ECG Case Studies

My department is starting a 12-lead ECG "case of the month" as part of our continuing education. Each month, I will select an ECG that was transmitted from the field and resulted in a cath lab activation.

Whenever possible, I will include the "before" and "after" angiograms so that the paramedics receive feedback about the culprit artery. A "clinical pearl" will also be included whenever it seems appropriate.

Here are the first two case studies. Followers of this blog will recognize the ECGs and angiograms. Going forward, I will document the E2B and D2B times.

Your feedback is welcome.

HHIFRD STEMI Program - September 2009 Case Study

View more presentations from tbouthillet.

HHIFRD STEMI Program - October 2009 Case Study

View more presentations from tbouthillet.

False positive cardiac cath lab activations - PowerPoint

Here's an interesting PowerPoint presentation that corresponds to a previous post.

False positive cardiac cath lab activations

I found slide 14 to be particularly interesting.

False Positive Cath Lab Activatin C R T Version

View more presentations from momiamd.

This is a topic that doesn't get enough attention. Often the quarterly STEMI meetings go over the success stories but not the failures. It's often said that if you don't have any false positives you aren't trying hard enough.

I don't disagree, but they should be reported, and the ECGs should be analyzed for teaching points. Hindsight is 20/20 and I understand that, but very few 12-lead ECGs are more interesting than those that caused a false positive cardiac cath lab activation.

Find them, scan them, and post them! I can't think of a better educational tool than an archive of STE-mimics that actually led to a patient being emergenty cathed!

Speaking of false positive cardiac cath lab activations, read these comments by Sameer Mehta, MD, FACC, MBA in the Cath Lab Digest.

He says in part:

I cautioned against complacency towards proceeding with emergent cath/percutaneous coronary intervention (PCI), citing precisely the high false alarms that have been mentioned in this outstanding study reported by Dr. David Larson. By the American College of Cardiology (ACC)/American Heart Association (AHA) criteria for primary stenting, the rates for these ‘false alarms’ should be less than 15%. By this standard, the 14% of the false alarms cited by Dr. Larson at the Minneapolis Heart Institute Foundation at Abbott Northwestern Hospital is quite acceptable. Yet the authors have creditably deemed these rates as unacceptably high. The reader must also be made aware that the Minneapolis experience, with its Spoke and Wheel, pharmaco-invasive model of triage for primary PCI is one of the most advanced programs in the world, and one that has established superb guidelines and pathways for very effective triage for STEMI patients. I emphasize the excellent caliber of the work at Minneapolis Heart Institute since their high false alarm rates may actually be some of the lowest in the nation, and that the problems of these false alarms may be much higher at other institutions, in particular, at low-volume STEMI institutions...

There are several ways for individual institutions to get their arms around this burgeoning problem. It is obvious that the emergency department (ED) physicians are under great stress to diagnose STEMI – they have to be very accurate and very fast. It is a new responsibility that has been assigned to them quite rapidly...

[S]everal contributing authors as well as I have strongly emphasized the need to monitor the false alarm rates. We have declared these rates to be the best parameters of measuring the efficacy of a STEMI program...

[A]dministrations and medical staff must mandate high caliber for ED physicians that would participate in STEMI programs. Rigorous training in EKG interpretation is the cornerstone of this new role and continuous quality improvement (CQI) processes must be rigid in this assurance. To be perfectly candid, if any institution cannot provide such quality ED physicians, it has no business in declaring its ability to perform 24/7 STEMI interventions. In a situation where the high accuracy of the ED physician cannot be ensured, the institution must seriously consider to reverting to the time-tested method of the cardiologist evaluating the presenting EKG.

In STEMI Interventions: Managing the Chaos (transcript in .pdf) found at theheart.org, Tim Henry, MD gives a different perspective:

[E]ven the issue of false-positives is of some debate. For instance, Dr. Dave Larson who works with me had a very nice paper in JAMA a year ago that looked at this. We found that 14% of our patients don't have a clear culprit artery, but of those patients, there are about 40% who have positive enzymes. So there are other things that cause acute STEMI that are not necessarily related in need PCI. For instance, you can have spasm, you can have thrombus that resolves, and you can have stress cardiomyopathy. There are a variety of things that can do it. So if your patient has true ST-elevation and positive enzymes it's hard to call that a false positive. So, I just think that what you do is a true false-positive rate, using it with ED and paramedic activating the cath lab is really between 6% to 8%, which we certainly think is acceptable.

It's an interesting debate, and one I think we're going to be hearing more about as D2B times below 90 minutes become commonplace in the wake of the D2B Alliance and AHA Mission: Lifeline.