Intermittent third degree heart block due to stuttering inferior STEMI

A 71 year old male complained of near syncope and SOB without any chest pain.  His pulse was slow.  He was put on the monitor.  Here is the rhythm strip:

There is 3rd degree AV block at a rate of 48

A 12 lead ECG was recorded about 5 minutes later:

Sinus rhythm at a rate of 60, with a normal PR interval, and right bundle branch block with no ischemia.  There are inferior Q-waves diagnostic of old inferior MI.  The upright T-waves in V1-V3 are slightly unusual for RBBB, but nondiagnostic.  It is not known whether RBBB is new or old.


21 minutes later the patient became bradycardic again, so this ECG was recorded:

There is 3rd degree AV block at a rate of 43 (again), still with RBBB but now with an obvious inferior STEMI.  There is also some ischemic ST depression in V5 and V6.  The sinus node has a rate of about 75, so there is no excess vagal tone, and therefore no utility of atropine.


One might think that because there is associated RBBB, that it is infranodal AV block.  But the RBBB was present when the block and ST elevation were not, so it is likely a baseline feature of this patient's ECG.  Furthermore, inferior STEMI is much less likely to cause infranodal block.  The blood supply to the AV node is from the RCA, and the infranodal (HIS bundle) area is supplied by the LAD.  Therefore, intranodal (in the AV node) block is much more likely than infranodal (below the AV node, in the bundle of HIS).

When in the node, AV block has a much better prognosis than when below the node.    

In the setting of STEMI, the ACC/AHA guidelines, page 618, recommend permanent pacing as a Class I indication for:

1. persistent second-degree AV block in the His-Purkinje system (infranodal) with bilateral bundle-branch block or third-degree AV block within or below the His-Purkinje system after STEMI. (Level of Evidence: B)

2. transient advanced second- or third-degree infranodal AV block and associated bundle-branch block. If the site of block is uncertain, an electrophysiological study may be necessary. (Level of Evidence: B)

3. persistent and symptomatic second- or third-degree AV block. (Level of Evidence: C)

Persistent here is important, because it is likely that, after opening the artery, the block will resolve, and thus will not be persistent.

The patient was comfortable while supine, even with 3rd degree AV block.  The block was intranodal.  The patient would soon have PCI.  So no pacing was necessary.  One should have external (transcutaneous) pacing at the ready in case of worsening block, but with inferior STEMI this is unlikely to be necessary.

He went to PCI and had a mid-RCA occlusion opened.  Here is his post PCI ECG:

Sinus rhythm without any AV block.  ST elevation is resolved and there is inferior T-wave inversion (reperfusion T-waves).  RBBB is persistent, the T-waves and ST segments are more normal for RBBB.  Is this normalization after resolution of ischemia?  Or is this T-wave inversion due to reperfused posterior MI?  Without a previous ECG, it is hard to know for sure.

 

Initial troponin I was 0.035 ng/ml (99% reference, 0.034) and peaked at 13.4.  Echo showed infero-postero-lateral wall motion abnormality.

Learning points:

1. STEMI does not always have chest pain or SOB.  It is wise to obtain serial ECGs when there are ischemic symptoms, and especially with AV block.

2. Inferior STEMI may cause AV block, but it is intranodal

3. Infranodal AV block, especially in the context of anterior STEMI, is very dangerous and will probably require internal pacing unless the artery can rapidly be opened. Before the artery is opened, it is at least likely to require external pacing.

Interesting new paper: in this study, even interventionalists had a hard time differentiating non-ischemic ST elevation from STEMI

Reference:  Tran V, Huang HD, Diez JG, et al. Differentiating ST-elevation myocardial infarction from nonischemic ST-elevation in patients with chest pain. Am J Cardiol 2011;108(8):1096-101.

Here is a link to the pdf.

Here is a summary:

The authors (cardiologists) looked at the ECGs and records of 240 consecutive cath lab activations for STEMI (primary PCI, pPCI).  They excluded patients with LBBB or paced rhythms and others whose STE criteria did not meet guideline-based criteria for acute STEMI.  They did detailed chart reviews to determine if there was or was not actually a STEMI, in retrospect (looked at cath results, echos, biomarkers, etc.).  They then showed the ECGs to 7 experienced interventional cardiologists and asked them to interpret the ECGs and asked whether they would recommend immediate pPCI, assuming that the patient had appropriate ischemic symptoms.  They were blinded to outcome and other patient data.

Of 84 subjects, there were 40 patients with a true STEMI and 44 without (13 of whom had NonSTEMI).  Recommendations for immediate PCI varied widely, from 33% to 75%.  Sensitivities were 53% to 83% (mean, 71%), specificities 32% to 86% (mean 63%), PPV 52%-79% (mean 66%) and NPV 67% to 79% (mean 71%).  When the readers chose non-ischemic ST elevation, LVH was thought to be the cause in 6% to 31% and old MI/aneurysm in 10% to 26%.

They show some very interesting tracings which are very similar to many I have shown on this blog.

This adds to the growing evidence that even among the "experts", ST elevation is very difficult to diagnose.

A previous study by Turnipseed et al.(1) showed that early repolarization was frequently misdiagnosed as STEMI and vice versa.  Cardiologists performed slightly better than emergency physicians.  Jayroe et al. (2) distributed difficult ECGs to 15 "expert" electrocardiographers and found that they had difficulty distinguishing STEMI from nonischemic ST elevation.

How would emergency physicians perform?  Or paramedics?  This is unknown, but to some extent it is much more important to those of us on the front line, and I wouldn't be surprised if many spend more time studying ECGs and are more expert than interventionalists.  The interventionalist has to respond to a cath lab activation.  The paramedics and EPs need to actually make the decision to activate.  We should have a lot of motivation to learn the differences between the true positives and the false positives.

Christopher Watford posted some very interesting data below.  I'll post part of it here:

---Dr. Paul R. Hinchey, Austin-Travis County's medical director, had a presentation at the 2012 Gathering of Eagles conference (presentation is available online) where he discussed the practical implications of using Cardiology to overread EMS 12-Leads. His service had received complaints due to the number of "false activations" given by his Paramedics.

---Dr. Hinchey implemented standardized activation criteria and had a panel of 3 cardiologists over-read the EMS activations to determine appropriateness, his findings were as follows for 90 EMS STEMI alerts:

- 87% (74/90) Positive to at least 1 cardiologist
- 63% (57/90) "True" Positives (2 of 3 cardiologists agreed)
- 43% (39/90) Unanimous "True" Positive
- 37% (33/90) "False" Positives (2 of 3 agreement)
- 18% (16/90) Unanimous "False" Positive

Bottom line: there is a long way to go in getting better at interpreting ST elevation on the ECG.  Rules to help do so could prove very valuable.  Some such rules already exist, such as the early repol vs. anterior STEMI rule and the LV aneurysm rule.

Early repol rule:  Strictly speaking, this was not studied in ECGs with: 1) T-wave inversion, 2) coved (upwardly convex) ST segments, or 3) LVH.  Here is the formula; there is an excel spreadsheet down the right side of this blog: (1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).  A value greater than 23.4 is quite sensitive and specific for LAD occlusion.

LV aneurysm rule:  There is one retrospective study (Smith SW. American Journal of Emergency Medicine 23(3):279-287, May 2005) showing that the T/QRS ratio is significantly greater in acute anterior STEMI than in old anterior MI with persistent ST Elevation. The best criterion for differentiating was the sum of STE in V1-V4 divided by the sum of the QRS's in V1-V4 (TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4). If this value was greater than 0.22 vs. less than 0.22, then it is likely to be acute STEMI.  Another rule that was almost as good: if any one of the leads had a ratio of T to QRS greater than, vs. less than, 0.36, it was very likely to be STEMI.

References:

1. Turnipseed SD, Bair AE, Kirk JD, Diercks DB, Tabar P, Amsterdam EA. Electrocardiogram differentiation of benign early repolarization versus acute myocardial infarction by emergency physicians and cardiologists. Acad Emerg Med 2006;13(9):961-6.)

2. Jayroe JB, Spodick DH, Nikus K, et al. Differentiating ST elevation myocardial infarction and nonischemic causes of ST elevation by analyzing the presenting electrocardiogram. Am J Cardiol 2009;103(3):301-6.

Benign T-wave Inversion: view video or read text

Benign T-wave Inversion from HQMedEd on Vimeo.



There are many etiologies of T-wave inversion.  We are most worried about ischemic T-wave inversion.  Wellens' syndrome is particularly dangerous, as it signifies an unstable critical LAD stenosis.  I have several posts on this; here is one that shows the entire evolution.

Another etiology is "Benign T-wave Inversion", which has long been recognized. I first saw it described in Chou's textbook.  It is a normal variant associated with early repolarization.  K. Wang recently studied it.  He reviewed ECGs from all 11,424 patients who had at least one recorded during 2007 at Hennepin County Medical Center (where I work) and set aside the 101 cases of benign T-wave inversion.  97 were black.  3.7% of black men and  1% of black women had this finding.  1 of 5099 white patients had it.  Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group.

I have reviewed these 101 ECGs, and what strikes me is:

1. There is a relatively short QT interval (QTc < 425ms)
2. The leads with T-wave inversion often have very distinct J-waves.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which evolves).
5. The leads with T-wave inversion (left precordial) usually have some ST elevation
6. Right precordial leads often have ST elevation typical of classic early repolarization
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
9. II, III, and aVF also frequently have T-wave inversion.

Below are 5 examples, followed by a case of Wellens.'

I show you the LAD-BER formula calculations, but remember, strictly speaking, this was not studied in ECGs with: 1) T-wave inversion, 2) coved (upwardly convex) ST segments, or 3) LVH.


Here is the formula; there is an excel spreadsheet down the right side of this blog: (1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).  A value greater than 23.4 is quite sensitive and specific for LAD occlusion.

Benign T-wave inversion: There is ST elevation in V2 and V3, with T-wave inversion in left precordial leads.  QTc = 395ms, formula value (to determine if the STE is STEMI or not) = 21.13 (< 23.4 is early repol).  Note the prominent J-waves, the minimal S-waves and the prominent R amplitude in leads with T-wave inversion.

Benign T-wave Inversion: This has some scary looking STE and TWI.  QTc is 415ms and formula value is 21.39.

Benign t-wave inversion.  QTc = 415, formula = 18.5

Benign T-wave inversion and probable LVH.  Scary ST elevation, right?  But QTc is 421ms and formula value is 20.17. 

Benign T-wave Inversion?  QTc 398, formula 17.6.  This one was not stable.  The next day it was gone.  It was recorded in a young black male with chest pain.  There were negative serial troponins but no angiogram.  Dr. Wang considered it to be BTWI.

Wellens' syndrome.   Note the evolution from A to C.  It begins with terminal T-wave inversion (biphasic) in lead V2, later extends to V3 and V4, and still later becomes deep and symmetric and only then extends to V6.  There was a critical LAD stenosis.  In this case I do not know what the computerized QTc was.  This is taken from an article I wrote in EM Clinics of North America 2006;24(1):53-89.

Weak, SOB, "DKA", Chest Pain, and Wide Complex Tachycardia: Is there STEMI?

This case was sent by a reader:

A 60 year old man presented with "DKA," Weakness, Dyspnea, and Chest pain with vomiting.  He denied fever or abdominal pain.

Heart rate was  in 150's, systolic BP in 90's, RR 30's, and pulse oximetry in the 90's.

He "looked gray".  His K was 5.2 and glucose 740 mg/dL.

He was acidotic: pH = 7.00, pCO2 = 25, pO2 of 78.

Here is his initial ECG:

There is a wide complex tachycardia.  If you look at V1, there is a narrow r-wave followed by a deep S-wave, typical of LBBB.  However, there are 4 narrow complex beats interspersed (see black arrows in image below).  Are these capture beats in the midst of VT?  If they were, they should come early, but they do not.  So is it VT or SVT with aberrancy?  That is a tough question.  If it is SVT with aberrancy or sinus with aberrancy, all I can surmise is that most of the time the left bundle is refractory at this fast rate, but in 4 instances it recovered in time to avoid LBBB.  The QRS duration is best seen in V1, where it appears to be only 120 ms. 

There have been a lot of interesting comments  on this ECG.  One is how V2 does not seem to fit between V1 and V3 and may be a misplaced lead.  Another points out the notch in descending limb of V1, which is one of Brugada's criteria for VT of the LBBB morhology type (see Brugada types below).  I am not 100% convinced of VT because of the apparently short QRS at 120 ms and I initially favored sinus with aberrancy and obscured p-waves, but have received some contrary feedback which you can read below in the comments section.  The bottom line is I am not certain if it is VT or not.

Brugada criteria for regular wide complex rhythm:
In Brugada's derivation sample, the sensitivity and specificity were 99% and 97%, but subsequent validation studies have not confirmed this. As an example, Vereckei et al. compared Brugada to his two algorithms and found Brugada's to be 86% accurate compared to 91% accuracy for the two Vereckei algorithms.


1. Is there absence of RS complex in all leads V1-V6? (concordance)
--If yes, then VT
2. Is interval from onset of R-wave to nadir of the S > 100 msec in any precordial leads?
--If yes, then rhythn is VT. If no, step 3
3. Is there AV dissociation?
--If yes, then VT, If no, step 4
4. Are morphology criteria foor VT present (see image below)?
--if yes, then VT.


Here are the Brugada morphologies of VT:

Next you need to determine whether there is ST segment elevation or depression. 

I have annotated the same ECG here:

The black arrows are the interspersed narrow complex beats.  It is easy to find the onset of the QRS in V1.  From V1, I draw black lines up to demonstrate the onset of the QRS in the other leads.  The red lines are the end of the QRS.  As you can see, there is concordant ST elevation or excessively discordant ST elevation in several leads.  II, III, and aVF have massive excessively discordant STE, diagnosing inferior STEMI.  There is excessively discordant reciprocal ST depression in leads I and aVL, confirming this.  V2 has concordant ST depression, diagnosing posterior STEMI.  V3 through V6 have excessively discordant STE or concordant STE, diagnosing anterior STEMI as well.

How could there be both inferoposterior and anterior STEMI?  There are three possibilities:

1) this is an LAD with a "wraparound" Type III LAD that feeds the inferior wall
2) there is either an LAD or RCA occlusion, but shock is so severe that the other wall has severe demand ischemia with ST elevation.
3) there is no acute thrombotic occlusion, rather there is only severe demand ischemia from shock, extreme tachycardia, and fixed coronary stenoses.

The second ECG was similar but without the few narrow complexes:

Then the patient rolled over, vomited, and became unresponsive.  He was cardioverted, intubated, had a bradycardic arrest, chest compressions, and epinephrine, and was resuscitated.

Some time during this, this ECG was obtained:

The rate is 220 and it is very wide.  This is clearly ventricular tachycardia.

After resuscitation, this ECG was obtained:

Now there is a narrow complex. There is only inferoposterior STEMI now, with additional ST elevation in V4 and ST depression in V5 and V6.  The rate is 164.  It is hard to say whether this is sinus.  The upright p-wave in V1 suggests atrial flutter with 2:1 block and the second flutter wave hidden in the QRS, but it is difficult to correlate that in lead II.

The cath showed a proximal RCA occlusion and severe 3 vessel  disease.  Unfortunately, he expired the next day.


Here is the VT discussion:

Vince D, Mar 18, 2012 02:26 PM


While I'm very tempted to take opinion of Dr. K. Wang as inherently correct, I still get the sense that those are fusion beats of some sort in tracing #1. Here's what's spinning around in my head at the moment:

1)The initial deflection of each narrow complex matches that of its wide brethren, common for fusion.

2) Although it is an extremely regular tachycardia, and it's true that the narrow beats don't arrive early, the complex immediately following a narrow beat is consistently just a little ahead of schedule, with the following beats shifting forward in time accordingly. This suggests that the entire mechanism of the tachycardia is affected by each fusion.

3) There seems to be a relationship between the narrowness of the complexes and how early the next beat arrives. I'm far from an expert at such things, but points 2 and 3 have me leaning towards some sort of re-entry for the underlying mechanism. It's not just a single early beat following the "event" as in enhanced conductivity. I've only looked at a couple of cases of V-Tach with fusion beats, but this pattern seems to match. I haven't taken the time to compare it to other automatic or re-entrant arrhythmias.

4) Although the morphology is a bit different, the QRS axis of the apparent V-Tach in tracing #3 very closely matches tracings 1 and 2 in both the frontal and precordial planes.

5) In most leads with clear R or S waves, they are slow to reach their peak or nadir.

At the beginning of this comment I was very skeptical of the initial tracings being V-Tach and just meant to bring up my a point of dissonance for me. At this point, however, I have a pretty strong suspicion that V-Tach is actually the diagnosis. Thoughts, or am I off-base?


I will note that my initial suspicions revolved around the idea of the narrow beats being the fusion of LV PVCs in the face of a supra-ventricular rhythm with LBBB, but I just couldn't rectify that with the other findings. I especially wanted it to be a parasystolic LV rhythm, but the irregularity of their appearance nixed that idea early.



Reply
Steve Smith, Mar 18, 2012 04:09 PM

Vince, you're not at all off base.

Your arguments are sound and it very well could be VT. I don't think it's a slam dunk either way.

One argument against a rate-related LBBB is that the rate is yet faster in the last ECG, but there is no BBB.

One argument against VT is that you would have to say there are two different VT morphologies in this patient (the first and third EKGs). You thought they are similar morphologies? To me they look very different.

If these are fusion beats, and I understand your arguments in favor, then on all 4 the supraventricualar beat arrives at exactly the same time as the ventricular beat. This is possible but very unusual. It is unusual to see even one fusion beat in VT, much less 4, but then this is in any case an unusual ECG.

I tried applying some of the rules, for instance, Sasaki (not validated, and none of the rules are really excellent):

Step 1: Initial R in aVR?

This means is there a large single (upright) R-wave (not a small r-wave) in aVR. This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.

--If yes, then rhythm is VT. If no, step 2.

Here the answer is NO.

Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?
--If yes, then rhythm is VT. If no, step 3.

Here I get a maximum of 80 ms. So NO.

Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)

--If yes, then it is VT. If no, then it is SVT. "No" here, therefore it is SVT

I see only one lead where there is an initial r- or q-wave of about 40 ms, and that is aVR. So the answer here is also NO.

Then you have to figure in the low pH, which can alter conduction.

In any case, whether VT or not, the STEMI is evident. And when in doubt, shock a fast rhythm in an unstable patient.

Steve Smith

Wide Complex Tachycardia after Ingestion and Seizure

A young man presented after a prolonged seizure. He had had a fight with his girlfriend, and she thinks he ingested something, thinks it was ecstasy (MDMA) but might have been other things.

The patient was unconscious.  He was intubated.  He had a combined respiratory and metabolic acidosis, with pH 6.98, pCO2 of 65 and HCO3 of 15.  K was normal. Blood pressure was 180/80.   There was no pulmonary edema or hypoxia.  Cardiac Echo showed excellent hyperdynamic function.  Here was his initial ECG:

Regular Wide Complex Tachycardia.  The computer read the QRS duration as 160 ms. 

Approach to Wide Complex Tachycardia

Unstable – Shock it

12-lead if at all possible

   --Unstable defined by:

• Chest Pain
• Shock
• Hypotension
• Very dyspneic 
• Pulmonary Edema

Stable

• Get a 12-lead ECG
• Sinus?
• You have little to lose by shocking (safe even if sinus, but best not to shock sinus tach)
• Must be able to safely do procedural sedation
• If converts, then recurrence after cardioversion requires antidysrhythmic medication

 This patient had an ingestion and seizure, is young and has a hyperdynamic heart with good function.  He could have VT due to his ingestion, but sinus tach is far more likely.

Here is the same ECG with some annotation (lines):

The first line is drawn at the onset of the QRS in V2, which is clear.  I draw this down to the bottom lead II rhythm lead to show where the onset of the QRS is in lead II.  Then you can draw analogous lines for all other leads.  The QRS duration appears to be closer to 120 ms, arguing strongly against VT.  There is a superior axis (about -90 degrees).  The duration from the onset of the R-wave to the nadir of the S-wave in V2 and V3 is about 60 ms, which argues strongly against VT.  There is a tall R-wave in aVR, consistent with sodium channel blocking effects of toxins.  This is unlikely to be VT.

The clinicians shocked the patient at 200 J x 2, with no change.  They administered sodium bicarb as antidote for Na channel blocking effect.  Then, with supportive care and fluids, over the next 10 minutes, the heart rate slowly and gradually decreased to 150.  Here is the subsequent ECG:

This is clearly sinus tach.  The QRS duration has shortened a bit, but there is still a large R-wave in aVR.  The axis is still superior.  The morphology of the QRS has not changed, confirming that the previous rhythm was supraventricular.

In this case, the first ECG has no obvious p-waves, but they may be there and difficult to discern.  As the patient is not hemodynamically unstable, it is reasonable to give some supportive care and wait to see what happens.  When the rate gradually falls, as in this case, then it must be an automatic, not re-entrant, rhythm.  Re-entrant rhythms are constant, though can be affected by antidysrhythmics.

That the morphology of sinus is the same as in the initial ECG makes an SVT, including sinus, definite.

That it fell gradually strongly supports sinus as the initial rhythm.

Outcome: the patient recovered uneventfully.  The drug screen, including chromatography for 4000 different substances, was negative for all except pseudoephedrine.  However, many toxins do not show up on tox screens.





Differential of Wide Complex Tachycardia (check out this post)

--Sinus with aberrancy -- Aberrancy can be due to toxins (wide complex from the many drugs which have sodium channel blocking effects and prolong the QRS)
--SVT with aberrancy.
--VT

Assess pretest probability:

--Majority of wide complex tachycardia is VT

--If h/o MI, cardiomyopathy, low Ejection Fraction, VT more likely still

Assess the ECG:

--P-waves in front of QRS? --Sinus

--Irregularly irregular? A fib (V tach is regular)

--Regular? --then: sinus / atrial tach / flutter / PSVT / VT)

--Rate gradually changes or always the same?

              Gradual: sinus

              Unchanging: reentrant rhythm such as: flutter vs. PSVT vs. VT

--Look for a true bundle branch block pattern:

              Right or left (sinus or SVT with aberrancy)

--Fusion beats (occasional narrow complex fused with wide one)

              Almost always VT, but not always

--QRS > 140 ms favors VT
--Concordance in precordial leads (no RS in any lead)

Consider Adenosine if you think it is SVT with aberrancy

--safe in VT
--safe in WPW, if regular rhythm
--Unsafe in WPW with atrial fib
--converts reciprocating tachycardia, whether orthodromic or antidromic
    --these depend on the AV node for re-entrance
--converts one kind of fascicular VT

4 Algorithms to differentiate SVT with aberrancy from VT

Brugada, Vereckei 1, Vereckei 2, Sasaki

 Here is my presentation of Sasaki's rule.

First 3 are complex and I find difficult to apply.  All (except Sasaki's, for which as far as I know there has been no validation attempt) have fared substantially worse in validation than in derivation.   

I put in a little effort to make the diagnosis based on these algorithms, but don’t obsess on it.

Management

If you're not sure, but pretty sure it is not sinus tach

Sedate/Cardiovert (or Adenosine)

Adenosine if you suspect SVT:

---Older, with known absence of structural heart disease

---Young age, unless known heart disease

---QRS < 140 ms

---No obvious signs of VT

       concordance, fusion beats, AV dissociation

---Unequivocal rapid depolarization of the initial part of the QRS (e.g., normal LBBB or RBBB)