This is a 68 yo male with a history of aortic stenosis, on carvedilol, fell from a ladder approx 20 ft onto concrete, landing face down with likely loss of consciousness. Upon EMS arrival, pt was still face down in a pool of blood, but was responsive, alert, and neuro intact. His BP was stable en route, but he was bradycardic in the 30's.
On exam, he had multiple orthopedic injuries, but no significant head, neck, spinal, chest, or abdominal injuries. The patient had had no premonitory chest pain or SOB. His BP was 121/59 and he was well perfused. This was his initial ECG:
First troponin returned at 0.11 ng/ml (slightly elevated). With all his injuries, he spent 2 hours in the ED, and a subsequent ECG is shown here:
This is a classic ECG. A drop attack with third degree AV block is called a "Stokes Adams" attack, and is often associated with bizarre wide inverted T-waves. A google scholar search comes up with several articles: Giant T-wave inversion associated with Stokes-Adams syncope (sycope due to complete AV block).
The escape rhythm is dependent on the automaticity of the tissue that escapes. AV nodal escape is the fastest, then HIS bundle, then Purkinje fibers, then ventricular tissue (which results in a slow "idioventricular" rhythm)
In this case, there is either an alternating escape, or a nodal escape with alternating RBBB and LBBB. If it is the former, then you know that your bundles have appropriate automaticity and can support the rhythm without a stimulus from above. If it is the latter, then you have the risk of developing block of both the left and right bundles simultaneously, in which case the only escape possible is idioventricular.
Obviously, this is a dangerous situation, and you must place transcutaneous pacing pads and ascertain that they will capture if you need them too. Alternatively, an internal pacing wire can be placed.
A simple test of capture is nicely done by pacing and observing the heart with bedside ultrasound to be certain of capture.
Case continued:
Fearing possible beta blocker toxicity, glucagon was given in increments up to a total dose of 5 mg, but this was not effective. Atropone 1 mg was given without effect (this will not work in this situation, ever). An internal pacing wire was placed in the ED, but not used because, in the interim, dopamine had been started and titrated to 10 mcg/kg/min with an increase in the heart rate to the 50's. Pacer pads were also placed.
Subsequent troponins rose to a maximum of 8.5, suggesting that ACS may have had a role here. However, third degree heart block can develop for other reasons than acute MI.
An echocardiogram revealed moderately severe aortic stenosis with a valve area of 1cm2, with a mean pressure gradient of 50mmHg. There were regional wall motion abnormalities (apex, distal septum and
inferior) but these are difficult to interpret in the setting of LBBB.
Angiography and Ventrilography revealed worse AS, with valve area of 0.74 cm2. There was no coronary artery disease.
A permanent pacer was placed on hospital day 3.
This is the final ECG:
After many orthopedic procedures, the patient had his aortic valve replaced, and went home.
On exam, he had multiple orthopedic injuries, but no significant head, neck, spinal, chest, or abdominal injuries. The patient had had no premonitory chest pain or SOB. His BP was 121/59 and he was well perfused. This was his initial ECG:
 |
| There are regular p-waves at a rate of about 90, but they do not conduct. Thus, there is 3rd Degree AV block with a probable Purkinje escape at a rate of 36; the wide QRS and RBBB pattern (rSR' in V1, wide S-waves in lateral leads) tell us that the escape is from the left bundle, creating an RBBB-like ECG. [Alternatively, there could be a nodal escape with RBBB]. There are also very wide, bizarre, inverted T-waves. The QT is 680 ms, and QTc = 527 ms. There are no ST changes indicative of STEMI. |
First troponin returned at 0.11 ng/ml (slightly elevated). With all his injuries, he spent 2 hours in the ED, and a subsequent ECG is shown here:
 |
| Now the escape has an RBBB in the first part of the ECG, and LBBB pattern in the latter part, and the rate is 41. The escape has alternated to the right bundle [or there is a nodal escape with LBBB]. |
This is a classic ECG. A drop attack with third degree AV block is called a "Stokes Adams" attack, and is often associated with bizarre wide inverted T-waves. A google scholar search comes up with several articles: Giant T-wave inversion associated with Stokes-Adams syncope (sycope due to complete AV block).
The escape rhythm is dependent on the automaticity of the tissue that escapes. AV nodal escape is the fastest, then HIS bundle, then Purkinje fibers, then ventricular tissue (which results in a slow "idioventricular" rhythm)
In this case, there is either an alternating escape, or a nodal escape with alternating RBBB and LBBB. If it is the former, then you know that your bundles have appropriate automaticity and can support the rhythm without a stimulus from above. If it is the latter, then you have the risk of developing block of both the left and right bundles simultaneously, in which case the only escape possible is idioventricular.
Obviously, this is a dangerous situation, and you must place transcutaneous pacing pads and ascertain that they will capture if you need them too. Alternatively, an internal pacing wire can be placed.
A simple test of capture is nicely done by pacing and observing the heart with bedside ultrasound to be certain of capture.
Case continued:
Fearing possible beta blocker toxicity, glucagon was given in increments up to a total dose of 5 mg, but this was not effective. Atropone 1 mg was given without effect (this will not work in this situation, ever). An internal pacing wire was placed in the ED, but not used because, in the interim, dopamine had been started and titrated to 10 mcg/kg/min with an increase in the heart rate to the 50's. Pacer pads were also placed.
Subsequent troponins rose to a maximum of 8.5, suggesting that ACS may have had a role here. However, third degree heart block can develop for other reasons than acute MI.
An echocardiogram revealed moderately severe aortic stenosis with a valve area of 1cm2, with a mean pressure gradient of 50mmHg. There were regional wall motion abnormalities (apex, distal septum and
inferior) but these are difficult to interpret in the setting of LBBB.
Angiography and Ventrilography revealed worse AS, with valve area of 0.74 cm2. There was no coronary artery disease.
A permanent pacer was placed on hospital day 3.
This is the final ECG:
 |
| Perfectly normal paced rhythm. Note that all precordial QRS are negative. This is because the pacing lead is placed in the apex of the right ventricle, so that depolarization always proceeds away from the apex of the heart (on the chest, the point of maximal impulse). Thus, it depolarizes away from all precordial leads. |
Awesome case, thank you! I had one very similiar last autumn, she was out for 20 seconds (captured on telemetry) and had general anterior T inversions. My first thought then was Wellens and I almost turned pale when I saw they sent her home with pacemaker but did no angio... So your case explains it all!
ReplyDeleteYour case fits the Wellens criteria quite well though;
* Symmetric, deep T wave inversion or biphasic T waves in V2-V5 or V6 during pain free periods
* No precordial Q waves or loss of R waves
* Minimal (<1mm), if any, ST elevations
except for missing chest pain of course but with the elderly you never know... However a syncope would not be explained by critical LAD stenosis unless there was decreased contractility (hypotension) or AV/SA node problem but this obviously is a bundle branch conduction problem and thus unlikely. Am I right?
BTW, what do you think is the physiological explanation behing the T inversions?
David,
ReplyDeleteIt does fit with Wellens' but the T-waves are much more bizarre (wide and deep). Critical LAD stenosis could cause syncope for many reasons: AV block, sudden poor contractility, VT. But here the reason stares us in the face with AV block. And we know from the literature that this happens. However, I don't think I would send someone home without a cath unless the troponins were negative, which I think would be very unlikely. There was ischemia (infarct, in fact) in this case due to the supply demand mismatch (type II MI) from both Aortic stenosis and bradycardia. These T inversions are at least partly due to ischemia, but I don't know if there is something else about this syndrome. I suspect it is a form of stress cardiomyopathy. The diffuse T inversions are similar to that.
Steve
Thank you for the wonderful case Dr. Smith!
ReplyDeleteBroad symmetrical T waves are also known as neurogenic T's. Also with Wellen's the dr's I know are weary to diagnose it in a 3rd degree block. On the second 12 lead, and correct me if I'm wrong, it looks as though the first few beats are RBBB mimics and then turns into LBBB mimic.
The delivery of atropine in my opinion would worsten an MI due to the increased O2 demand, especially in a 3rd degree. Since it was demand ischemia I would have tried dopamine first then TCP (since I'm prehospital).
Again thank you for the awesome cases!
You're absolutely right about the 2nd ECG: it starts as RBBB and changes to LBBB in the same ECG. I'm going to edit the entry! I wouldn't worry about atropine and O2 demand, but dopamine greatly increases O2 demand. Atropine won't work anyway.
ReplyDeleteDear Dr Smith,
ReplyDeletewhen I first looked at the ECG, for a moment I thought it is SDH as pt had a fall. Is it true that with brain hemmorhage we tend to see large T wave inversion?
Amita,
DeleteYes, we do see bizarre T-wave inversions in intracranial hemorrhage when there is associated stress cardiomyopathy, but we don't see third degree heart block or these alternating blocks.
Steve Smith
this is a typical case presentation of pulmonary embolism in patient with pre existing LBBB
DeleteSalah,
DeleteI don't understand the comment. Completely inaccurate.
Steve Smith
It is interesting to note that the primary ECG fits the criteria of Shvilkin et al. for T waves of cardiac memory.
ReplyDelete1. T wave upright in lead aVL
2. T wave upright or isoelectric in lead I
3. Depth of deepest inverted precordial T wave exceeds that of lead III
Of course, however, the latter does not fit the clinical picture (I was simply looking at the ECG). Also, I would argue that QT prolongation is more a feature of neurogenic T waves and Adam-Stokes syndrome rather than cardiac memory.
Also, again just examining the first ECG without considering the clinical picture, by the findings of Kosuge et al., a T wave inversion in lead III makes ACS quite unlikely.
The cases you present are very interesting with a lot to teach. Excellent website, Dr. Smith.
Mamdouh KJ Jr.
4th-year medical student
Mamdouh,
DeleteYes, this is not a situation in which cardiac memory is relevant. Also, the Kosuge article was limited to patients who had either PE or ACS, so that should not be applied here.
Glad you enjoy the site and I hope it helps you manage your patients!
Steve Smith