Thursday, August 25, 2016

An Unusual Tachycardia

This Case was sent by Atif Farooqi and Scott Weingart, from Stony Brook.

This is a 70-something with history of CABG who presented with 30 minutes of SOB and palpitations.

Here is his ECG:
What is it?

Atif wrote this:
"My first thought was perhaps a bidirectional V Tach, though the pt is not on digoxin and otherwise has no discernable reason to be in BVT.  Scott was considering maybe an intermittent aberrant conduction, though we thought it odd for it to be strictly alternating beats.

Here is my answer:
Interesting EKG!
I think it is SVT with every-other-beat-aberrancy. 
--Every QRS comes right on time, perfectly regular, so it can't be Bigeminy. 
--Every other beat is RBBB, which is the most common type of aberrancy because the right bundle has a longer refractory period than the left.
--The inbetween beats are of normal duration (100 ms).  The axis does not alternate.  There is no alternating RBBB and LBBB.  So it can't be bidirectional tachycardia (neither bidirectional VT nor bidirectional SVT).
--There are no P-waves.
So this is AVNRT with alternating aberrancy (Scott was right!).

Additionally, both the aberrant and the normally conducted beats have significant ST depression.

Bidirectional Tachycardia implies alternating frontal plane axis, from -60 to +120, or alternating LBBB and RBBB.

Bidirectional tachycardia can be Bidirectional Ventricular Tachycardia, as with Digoxin toxicity.  The etiology may be:
1. alternating location of origin of the VT ectopic focus, or
2. alternating routes of depolarization from a single ectopic focus

Bidirectional VT may also result from aconite toxicity, as in this case I reported, which has alternating RBBB and LBBB.

Bidirectional Tachycardia can alternatively be due to SVT with Bidirectional Aberrancy:  the aberrancy may be due to:
1. RBBB with alternating LAFB (left axis) and LPFB (right axis), or
2. Alternating RBBB and LBBB.

Here is the ECG from this case of Aconite Toxicity:
Alternating RBBB and LBBB.  Intervals are regular.

This case presented here today does NOT have alternating frontal plane axis, nor does it have alternating RBBB and LBBB, so is not bidirectional tachycardia.

Case continued:

The attending gave IV Metoprolol, (the patient was supposed to be taking oral metoprolol as an outpatient), and the rhythm changed to the following: 
This appears to be sinus, though the P-waves are not obvious.
This subsequent ECG proves that the first was SVT with aberrancy: the complexes are identical to the non-RBBB beats of the first ECG.
There is also persistent ST depression.  Hopefully now that there is no longer tachycardia, this ischemia will resolve.

It is typical for metoprolol to convert an AVNRT. 
I would have tried adenosine.

Sunday, August 21, 2016

A 25 year old with Epigastric Discomfort, Worse Supine, Better Sitting Up.

This is another case provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club  

This is a 25 year old male diabetic who presented with epigastric heaviness for 12 hours.  The discomfort was intermittent and associated with sweating and dizziness; it was increased increased by lying flat and relieved when sitting up.

Here is his initial ECG, with pain and diaphoresis:

It is really quite normal.
When I first saw it, I did not know the patient still had pain, and I responded on FB:

"This is normal.  However, the sharp downturn of the T-wave in V4-V5 suggests possible development of Wellens' waves, but is nonspecific. The T-wave flattening in limb leads is non specific."
However, with ongoing pain, these are unlikely to be vestigial Wellens' waves.

He was given NTG and Morphine and pain was improved.

An interventionalist was consulted.  
He performed an echocardiogram which showed no wall motion abnormality.  

The first Troponin T returned at 0.017 ng/mL, slightly elevated but indeterminate.  

The interventionalist diagnosed pericarditis and prescribed an NSAID.

[This ECG shows no evidence of either pericarditis or of STEMI.  The diagnosis must have been based on the positional nature of the pain.]

Dr. Alwan smartly recorded more ECGs.   Here is the second one recorded 4 hours later:
No significant change

6 hours after the first ECG, and 2 hours after the 2nd, a third ECG was recorded:
Now there is new ST elevation, the change being diagnostic of LAD occlusion.
This is not an ECG one would see with pericarditis, which manifest inferolateral ST elevation.

Even if this were the first and only ECG, the differential diagnosis would be early repol vs. LAD occlusion, and the formula could be used:

STE60V3 = 2.5 mm
 computerized QTc = 437
(notice how it lengthened from the earlier values of 372 and 402 ms!)
R-wave amplitude V4 = 9 mm
formula = 25.839 (greater than 23.4 is all but diagnostic of LAD occlusion)

The patient was taken for angiogram.  Here is the report:

Here is the post reperfusion ECG
Typical reperfusion T-waves, identical to Wellen's waves (Wellens' waves represent reperfusion!)

Learning Points:

1.  Young People can have myocardial infarction
2.  Though positional pain lowers the likelihood that chest pain is MI, it does not eliminate it!
3.  Always get serial ECGs.
4.  Pay attention to even slightly elevated troponin levels.  This could have been myocarditis, but that is a diagnosis of exclusion, after a negative angiogram.

Thursday, August 18, 2016

Lecture: Acute Coronary Syndromes, Part (Overview and Non-STE-ACS) and Part 2 (STEMI)

Here is a pdf of all the slides (parts I and 2).
This contains some extra slides which were "hidden" in the presentation.

Part 1: Overview and Non-ST Elevation ACS

Part 2: ST Elevation Myocardial Infarction

Wednesday, August 17, 2016

A 50-something woman with atypical chest pain

This was provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club   

A 50-something female presented with atypical chest pain described as stabbing, with no radiation 
PMHx : DM poorly controlled 
VITAL signs stable 

Here is the initial ECG with the question "should the cath lab be activated?"
This is suspicious for ischemia because of the T-wave inversion in aVL.
However, this is very nonspecific and one would not activate the cath lab!

Another ECG was recorded 20 minutes later:
This has more obvious T-waves and T-wave inversion in aVL
Here is my response:
"This 2nd one is an extraordinarily subtle but real change!!" (i.e., this is diagnostic of MI).  "These often resolve with nitro, so I would try that first. It depends on your resources: if activating at night tires out your team for the next day, you try to avoid if possible.
But this pain and ECG may not resolve, in which case you must activate."

In other words, this is diagnostic of inferior MI, but not of STEMI, and may not need emergent cath lab activation.

If the pain and ECG findings resolved with nitroglycerine, it will need at least maximal medical therapy and continuous 12-lead ST segment monitoring

See these cases for the importance of ST segment monitoring:

A third ECG was recorded at 45 minutes:
Now it is unequivocally diagnostic of inferior MI, even though it does not meet millimeter criteria for inferior STEMI.
The cath lab must be activated.

Here are all 3 ECGs, one after another, so you can see the changes:

The cath lab was not activated, but a 4th ECG was recorded at one hour:
Now it meets STEMI criteria.
Cath lab was activated
What else do you notice?

There is also new ST elevation in V1.  So this is a right ventricular MI also

Echo: Basal inferior wall hypokinetic, pseudonormal LV filling pattern

Initial Troponin T: less than 0.01 ng/mL initial
Troponin T after 2 hours: 0.49 ng/mL

Troponin T after 4 hours: 1.6 ng/mL (this is a large MI)

Cath showed a 100% proximal RCA occlusion.

Learning Points:

1. T-wave inversion in aVL may be the first sign of inferior MI
2. Pay attention to slightly enlarged T-waves
3. When you see these subtle, nonspecific abnormalities, make certain you get serial ECGs!
4. Any patient with ongoing potentially ischemic chest pain should get serial ECGs!

Monday, August 15, 2016

What is this? A Perplexing ECG.

A 46 year old woman had syncope.  

Before seeing the patient or reading the chart, the physician viewed the ECG and was perplexed:
What is going on??

Then he found out she had a heart transplant.  Now can you tell what is going on?

It turns out that both the native heart and the transplanted heart are beating.  The native heart is paced by the transplanted heart.  The sequence is given in the legend of the annotated version below.

How does this work mechanically??

Both left ventricles pump blood into their respective aortas, then these two aortas converge immediately after their origins.  Thus, the hearts work in parallel, but the native heart beating slightly later than the transplanted one, and synchronized by the pacemaker. 

In this case, the patient had pulmonary hypertension.  If she had had a normal orthotopic transplant, the new right ventricle would not have been able to pump against the high pulmonary resistance.  Therefore, the native right ventricle pumps into the pulmonary artery, while the atria are connected (right with right and left with left).

The transplanted heart is over the native heart, with the apex directed rightward and upward (lead I, II and III are indeed negative). 

Annotated ECG:

Here I have drawn vertical lines at the beginning of each QRS:

The start of the native QRS is the first line
The start of the transplanted, paced QRS is the second line.

1. Transplanted heart P-wave 
2. Transplanted heart (abnormal) QRS (axis negative because heart is upside down!)
3. Native heart atrial spike (having sensed on the transplanted ventricle); no clear P-wave. 
4. Native heart ventricular spike followed by 
5. Native heart QRS. 

Wednesday, August 10, 2016

A Patient with Syncope

A young man had sudden syncope without a prodrome, after which he was aysmptomatic.  He presented to an ED and had this ECG recorded:
What do you see?

There is an abnormal rSr' in V1, with the r'-wave not falling quickly back to baseline.  The T-wave is inverted, but this is also a normal finding in V1.  The whole morphology is suggestive of Brugada morphology, but by no means "diagnostic" because the r'-wave is not 2 mm.

Here are the criteria for ECG Brugada morphology.  This comes from the paper entitled (with full text link): Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

Criteria for Type 1 Morphology:
1. R'-wave at least 2 mm in V1 or V2
2. But no distinct R'-wave because the ST segment takes off at an angle from the peak
3. The ST segment is convex upward ("coved"). [They use terminology of "concave downward"]
4. The peak at the high takeoff does not correspond with the J-point.  It is BEFORE the J-point, as measured in other leads (such as lead II across the bottom).
5. Gradual downsloping of ST segment such that at 40 ms after the takeoff, the decrease in amplitude is less than 4 mm.  In normal RBBB, the decrease in amplitude is much greater (see this example).
6. ST is followed by a symmetrically negative T-wave
7. "The duration of QRS is longer than in RBBB," and "there is a mismatch between V1 and V6." This criterion is perplexing and not well explained.
8. The downsloping should be such that the Corrado index is greater than 1.0.
This is the ratio: [ST elevation at the J-point] divided by [ST elevation at 80 ms after the J-point]. 

Diagnosis of Brugada Syndrome requires both:

1. Brugada pattern ECG (either Brugada Type 1, or the newly defined Brugada Type 2)
Findings may be dynamic and are sometimes concealed; findings may be observed only in certain circumstances such as fever, intoxication, electrolyte imbalance, presence of sodium channel medications/drugs, or vagal stimulation.
2. At least one of the following:
(a) survivor of cardiac arrest,
(b) witnessed/recorded polymorphic ventricular tachycardia (VT),
(c) history of nonvagal syncope,
(d) familial antecedents of sudden death in patients younger than 45 years without acute coronary
(e) Type 1 Brugada pattern in relatives.

Criteria for Type 2 Brugada morphology:
First, there must be:
a) An RSr' with a typical saddleback pattern in V1 and/or V2. 
b) V1 may have either an upright, flat, or inverted T-wave (in our case above it is inverted).
c) T-wave in V2 is usually but not always positive.
d) Minimum ST segment ascent of 0.5 mm.  There could be no saddle without an ascent.
Once these are fulfilled, there should be, in lead V2:
1.  High take-off of the descending limb of the r' at least 2 mm above the isoelectric line (in our case, it is less than 2 mm, so this does not meet criteria for Type 2 Brugada).   The r'-wave is thus not distinct, as it is in benign causes of rSr'
2.  Mismatch between QRS duration in leads V1 and V6 (longer in lead V1).  This helps to distinguish from RBBB, in which the QRS duration is equal in V1 and V6.
3. As with Type 1, the peak of the r'-wave does not correspond to the J-point in other leads.
4. A large Beta angle.  Go to this post to learn about the beta angle.

So this ECG cannot be said to fulfill the criteria for either type 1 or type 2 Brugada, but it is suggestive, and the patient had non-vagal syncope.

Case continued: 
The patient presented with syncope and fever 3 years later.  Here is the ECG:
Now the ECG, in the presence of fever, is diagnostic of Brugada morphology

The patient underwent an EP study and had a ICD implanted.

Learning Point:

The patient and doctor dodged a bullet here.  He could have died in the intervening 3 years.  This sort of cardiac syncope is death that terminates with awakening.

The first ECG is nonspecific but suggestive of Brugada, and in the context of non-vagal syncope the patient should at least get early referral to a cardiologist, preferably an electrophysiologist, for EP testing or for challenge with a sodium channel blocker.

Read more about Type 1 and Type 2 Brugada syndrome here:

Is this Type 2 Brugada syndrome/ECG pattern?

Here are many articles on Fever unmasking Brugada syndrome:

Friday, August 5, 2016

Proportionality and Serial ECGs Make the Diagnosis

This case comes from Jason Winter, of The Facebook Clinical Electrocardiology ECG Page.

A 60-something woman called EMS for chest pain.

Here is her first prehospital ECG:
What do you think?

There is very low voltage in the precordial leads, with a total QRS amplitude of only 3.5 mm in V2 and 4 mm in V3.  

In spite of this low voltage, there is ST elevation (as measured at the J-point and relative to the PQ junction, and as measured by the computer and shown on the right), of 0.54 mm in V2 and 0.65 mm in V3.   

The ST/QRS ratios in V2 and V3 are, respectively, 0.154 and 0.162.  These are a high ST/QRS ratios.  
In our study of subtle LAD occlusion vs. early repolarization, the mean ratio of ST/QRS was:

-- 0.215 and 0.195 for V2 and V3 in LAD occlusion vs. 
-- 0.077 and 0.081 for V2 and V3 in early repolarization.

The specificity of a value in V2 greater than or equal to 0.154 was 90% (90 of 100 cases).
The specificity of a value in V3 greater than or equal to 0.162  was 84% (79 of 94 cases).

However, we did not include cases with less than 1 mm of ST elevation, so strictly speaking, one should be circumspect about applying such ratios.  Nevertheless, these high ratios certainly suggest that there is abnormal ST elevation in the leads of the LAD territory.

How about if we apply the LAD occlusion/early repol formula?  
STE60V3 = 1
QTc = 397
RAV4 = 0.5 
This produces a value of 24.46 (greater than 23.4 is nearly diagnostic of LAD occlusion).  However, again, the formula was developed only in ECGs with at lead 1 mm of STE in V2 and V3, so does it apply?

Here is the same ECG stretched vertically so that the QRS amplitude is closer to normal:
Now one can appreciate the ST elevation a bit better.

Clinical Course

I don't know if the medics noticed these ECG findings or not, but if not, they recognized the value of serial ECGs in a patient with chest pain.

Here are these serial ECGs, starting with the first one again:

#1: Time zero:
STE in V2 and V3 = 0.54 and 0.65

 #2: 27 seconds later:
STE in V2 and V3 = 0.70 and 0.79

#3: 74 seconds after #2
STE in V2 and V3 = 1.11 and 1.21

#4: 56 seconds after #3:                 [157 seconds (2 min 37 sec) after the first]:
STE in V2 and V3 = 1.57 and 1.73

The medics administered aspirin (no Nitroglycerine), and the pain resolved.

#5: 18 minutes after #4:
STE is resolved

#6: 4 minutes after #5:
And remains resolved

Case Outcome

Because of ST resolution, the patient was not taken that night to the cath lab.  She was treated for NonSTEMI with antiplatelet and antithrombotic agents and went to cath the next day, where an where multiple LAD thrombi were found and the lesion will be stented.

Waiting to cath a transient STEMI can be hazardous.  See this case in which I made that mistake.

Learning Points:

1.  Repolarization (ST-T) is proportional to depolarization.  All ST elevation (and T-wave size) should be assessed relative the QRS amplitude.

2.  Serial ECGs improve the sensitivity of ST elevation on the ECG for MI.  In the only ED study of its kind, sensitivity increased from 46% to 62%.

Tuesday, August 2, 2016

Where is the lesion in this STEMI?

A middle aged male presented with chest pain.  EMS was called and an ECG was recorded which is virtually identical to the first ED ECG.

The cath lab was activated by the medics.

Here is that first ED ECG:
There is obvious inferior ST elevation, with reciprocal ST Depression in aVL (inferior STEMI).

There is also ST Depression in lead I.  This is good evidence that the inferior STEMI is caused by an RCA occlusion.

There is ST depression maximal in lead V2.  Thus, there is a posterior STEMI.

There is also ST depression in V5 and V6.

Where else is there evidence of STEMI?? (see below)?

There is absence of ST depression in lead V1.  Given the profound ST depression (of posterior MI) in lead V2, there should also be ST depression in lead V1, but there is not.  This suggests that something is "pulling up" the ST segment in lead V1.  In other words, there is relative ST elevation in lead V1.  As V1 sits directly over the right ventricle (RV), this suggests STEMI of the RV, which is caused by a proximal RCA occlusion, proximal to the RV marginal branch.

This patient did not have any of the hemodynamic characteristics of RVMI (hypotension, nitroglycerine sensitivity).

However, when I saw this I suspected RV MI and suggested to the treating physician that a right-sided ECG be recorded.

Here it is:
V1 should be labelled V1R, which is the same lead as V2
V2 should be labelled V2R, which is the same lead as V1
V3 is V3R
V4 is V4R
V5 is V5R
V6 is V6R
There is huge ST elevation across the right sided leads, diagnostic of RV STEMI.

Does this matter?  Won't the interventionalist just find the lesion and fix it?

Here is a case (in video form) in which the ST elevation in V1 was not noticed, a right-sided ECG was not recorded, and the angiogram showed occlusion of the mid-RCA, which was fixed.  When I called the interventionalist to ask about the proximal RCA due to STE in V1, he went back to look at the angiogram: what he had not noticed was that this occlusion was an embolus from the ulcerated plaque in the Proximal RCA.  He was thus able to go back and stent the actual culprit lesion.

Furthermore, it is good to know that the RV is involved in order to anticipate right sided heart failure with hypotension and nitroglycerine sensitivity.

How sensitive and specific is STE in V1 in the setting of RV MI, in cases with and without concomitant ST depression in lead V2?

We are just finishing a manuscript on this and cannot reveal our results.  Suffice it to say that STE in V1 is pretty specific but not sensitive.  Furthermore, that ST depression in lead I, though it does predict RCA occlusion, does not give any further information about whether that RCA occlusion is proximal (RVMI) or not.

In other words, all patients with inferior STEMI should have a right sided ECG recorded.

Saturday, July 30, 2016

Symptomatic Bradycardia. So-called Trifascicular Block. Occum's Razor and Hickum's dictum.

A middle-aged male with PMH significant for atrial fibrillation, cocaine use, DM, HTN, hyperlipidemia, and previous MI that was related to cocaine presented for 5 days of intermittent left-sided chest pain.  He reports that the pain is 10/10, sharp, non-radiating, and lasts for "a couple seconds," is associated with SOB and diaphoresis, and then dissipates/resolves on it's own.  Pain does not change with activity or position.   

Here is his initial ECG:
What do you see?

There is an irregular sinus bradycardia and both bifascicular block (RBBB and LAFB) and 1st degree AV block with a PR interval of 260 ms.  The last complex comes so late that there is a junctional escape before the P-wave can conduct.  However, every P-wave which gets the chance to conduct, does conduct.  There is no evidence of complete AV block.

 Bifascicular block + 1st degree AV block is inappropriately called "trifascicular block," a known misnomer.

Why is it a misnomer?  There is AV block and bifascicular block, but there are NOT 3 blocked fascicles as "tri-" implies.  If the right bundle, left anterior fascicle AND left posterior fascicle were all 3 blocked, that would be true trifascicular block and would be, by definition, complete ("third degree") AV block at the infra-HIS location.

However, it is true that when there is 1st degree AV block in addition to bifascicular block, it makes the AV block more likely to be below the bundle of HIS and makes subsequent complete heart block more likely.

Remember that RBBB and LAFB in the setting of STEMI implies a huge MI (from LAD or left main occlusion and is very dangerous.

Whenever there is high grade block and/or bradycardia, one must think of hyperkalemia and ischemia, and of course medications such as beta blockers and calcium channel blockers, although these latter will mostly cause sinus bradycardia and/or AV block, not block of the bundle of HIS.

The K returned, = 4.5 mEq/L.   Troponins were negative.   Here is the old ECG from 4 years prior:
"So-called" Trifascicular block was present then, but without the sinus bradycardia

This was recorded 22 minutes after the first:
There is profound sinus bradycardia, so much so that complexes 3, 4, and 7 are junctional escapes.

Overnight, it was reported that the patient had episodes of third degree AV block.

Here is the only 12-lead that was recorded:
There are no P-waves at all.  
One cannot call it sinus arrest for certain, because there is an escape at a rate of 38
(sinus arrest requires at least a 2 second pause, some say 3 seconds).

Such an escape is a bit too slow for a junctional escape, which generally happens at 40-60.

Furthermore, a junctional escape should have the same morphology as a conducted sinus rhythm.

However, this morphology is similar to RBBB with Posterior fascicular block, which implies an escape near the anterior fascicle.

Bizarre T-wave inversions (see link below)

Therefore, this is a ventricular escape rhythm.  The bizarre T-wave inversions are common in this situation. See this post:

Bizarre T-wave inversion of Stokes Adams attack (syncope and complete AV block), with alternating RBBB and LBBB

There is no evidence of third degree AV block here.

So this patient has 2 issues:

1) Complete heart block was seen on his monitor, but not recorded on a 12-lead
2) Long sinus pauses (which could be sinus arrest or simply sinus bradycardia, but since the escape happens before a 2-3 second pause can complete, one cannot be certain).

He did get an implanted pacemaker.

"Trifascicular" Block

For the reasons stated above, the 2009 AHA/ACCF/HRS scientific statement on the standardization and interpretation of the electrocardiogram recommends against using the term trifascicular block. 

Chronic bifascicular block in an asymptomatic individual (as this patient had 4 years prior) is associated with a low risk of progression to complete heart block. In contrast, a new bifascicular block with acute anterior myocardial infarction carries a much greater risk of complete heart block. 

Alternating right and left bundle branch block is interpreted as a sign of trifascicular block. In contrast, first degree AV block plus bifascicular block does notnecessarily indicate trifascicular involvement, since this combination can reflect slow conduction in the AV node with concomitant bifascicular block.

This 1981 Article from Circulation (volume 64(6):1265 (full text), studied patients with chronic asymptomatic bifascicular block (as in our patient above).  N = 329 with RBBB and LAFB, 46 with RBBB and LPFB, and 142 patients with LBBB.  These patients were divided, based on EP studies, into those with a prolonged (
greater than or equal to 56 ms) HIS-ventricle (HV) interval ( (n=319) vs. those with a normal HV interval (less than or equal to 55 ms, n = 198).   [A prolonged HV interval would result in a prolonged PR interval and the misnomer "trifascicular block" would be applied to these patients.]  Patients with prolonged HV interval were more likely to have evidence of organic heart disease such as cardiomegaly, CHF, PVCs, and angina.  Over a follow up period averaging 3.7 years, the development of true "trifascicular block," as defined by 2nd or 3rd degree AV block below the bundle of HIS, was 0.6% in the normal HV conduction group and 4.5% in the prolonged group.  

Thus, these patients with chronic asymptomatic bifascicular block and 1st degree AV block may have infra-HIS conduction delay (not just AV node delay).  Of course you do not know in the ED whether the delay is at the AV node or below the bundle of HIS without an EP study, but if they have organic heart disease, it is likely to be below the bundle of HIS.   These patients may indeed have an increased risk of complete AV block, but it is not imminent and does not need emergent treatment

However, if such a patient presents with symptoms as mentioned above (syncope, presyncope, weakness, etc.), then this condition may indeed be infra-HIS conduction delay with intermittent high grade AV block (causing intermittent symptoms) and require a pacer, or at least an EP study.

Our patient here is complicated by the fact that he also had severe sinus bradycardia, and possibly sinus pauses or arrest as the etiology of his symptoms (possibly sick sinus syndrome).  And then he reportedly developed complete heart block on the monitor in the hospital.  Thus, Occom's razor (look for only one unifying cause of a condition: Among competing hypotheses, the one with the fewest assumptions should be selected) did not apply, but rather Hickum's dictum ("Patients can have as many diseases as they damn well please.")

Here is another study of chronic bifascicular block showing low long term mortality in asymptomatic patients.

In this study of patients with RBBB and LAFB or RBBB and LPFB, there was a higher incidence of complete heart block, and 4 independent risk factors were found: Presence of syncope or pre-syncope, QRS greater than 140 ms, Renal failure, and an HV interval greater than 64 ms.

"After a median follow-up period of 4.5 years (2.16-6.41 years), a pacemaker was required by 102 patients: 45 had a ventricular pacing percentage >10% and 57 had significant AVB. Factors predictive of the need for a pacemaker were: the presence of syncope or presyncope (hazard ratio [HR]=2.06; 95% confidence interval [CI], 1.03-4.12), QRS width >140 ms (HR=2.44; 95% CI, 1.59-3.76), renal failure (HR=1.86; 95% CI, 1.22-2.83), and an HV interval >64 ms (HR=6.6; 95% CI, 4.04-10.80). The presence of all four risk factors was associated with a 95% probability of needing a pacemaker within 1 year of follow-up." 
Thus, it has been suggested that otherwise unexplained syncope in the presence of bifascicular block is an indication for a permanent pacemaker.   A randomized trial is ongoing.

Learning Points

1) Though chronic asymptomatic bifascicular block with first degree AV block (inappropriately named "trifascicular block") is infrequently associated with progression to complete heart block, and such progression generally takes months to years when it does, if a patient presents having had syncope, pre-syncope, weakness, dyspnea on exertion, or other symptoms compatible with unrecorded episodes of bradycardia, one must consider that these symptoms may have been due to intermittent complete heart block.

2) Look for and correct reversible causes: ischemia, drugs, and hyperkalemia.

3) If no reversible cause if found, one should consider placement of transcutaneous pacer pads in the ED.

4) If a patient with so-called "trifascicular block" develops complete heart block, it is likely to be infra-hissian (below the Bundle of HIS), and thus atropine will not work, and pacer pads MUST BE PLACED

5) Patients with a bradyarrythmia should be assessed for chronological incompetence: if you walk the patient down the hall, does his heart rate increase accordingly? Or does he get SOB and/or dizzy because his heart rate cannot accelerate accordingly?  The sinus rate should increase (AND of course there must be conduction of every P-wave.

Therapy of chronic bifascicular block with prolonged PR interval

1.  Look for and correct reversible causes: ischemia, drugs, and hyperkalemia
2. Permanent pacemaker in selected patients, including based on results of an EP Study