911 was called for a very elderly dialysis patient for acute onset of dyspnea.
On arrival, medics found the patient with agonal respirations. Chest compressions were started and 2 doses of epinephrine givne, and she was found to be in asystole, which then changed to PEA at some point, then to ventricular tachycardia. A King airway was placed.
This is her prehospital ECG:
On arrival, she was hypertensive and tachycardic. Due to concern for hyperkalemia, Calcium was given empirically. Cardiac ultrasound showed poor LV function and normal RV size. K returned at 5.8 mEq/L (not high enough to be responsible for all of this).
An ED ECG was obtained:
ECGs:
Prehospital:
--There is sinus tachycardia.
--The large R-wave in V1, with wide S-wave in V5 and V6 shows late forces toward V1 and away from V5 and V6, and is therefore diagnostic of right bundle branch block (RBBB).
--The large inferior S-waves, with a small q- and large R-wave in aVL are diagnostic of left anterior fascicular block.
--(Bifascicular block, RBBB and LAFB).
--Importantly, the PR interval is normal. If prolonged, there would be so-called trifascicular block.
These findings alone are very suggestive of LAD or left main occlusion. Every such case I have ever encountered was in a patient with either left main occlusion or LAD occlusion and the patient was near death or post-arrest.
This is a very bad sign, and the ST Elevation in these cases is frequently very subtle.
Finally, there are very large (hyperacute) T-waves in II, III, aVF and in V4-V6. These are diagnostic of either hyperkalemia or of acute STEMI.
ED ECG:
--Sinus tachycardia with RBBB and LAFB
--There is subtle ST elevation in V2-V5
Here the precordial leads are magnified:
RBBB should not have ANY ST elevation, so this is STEMI until proven otherwise.
In fact, in leads with a prominent R'-wave (here, as is usual: V1-V3), there should be ST depression that is discordant to the prominent R'-wave)
Here is an example of RBBB without any ischemia:
The ST elevation was not seen.
She had fever and elevated lactate.
Sepsis and pulmonary embolism were suspected.
CT pulmonary angiogram was negative.
After this, she had another brady-asytolic arrest and was resuscitated again.
Another ECG was obtained:
Further comment on this ECG:
--The ST elevation is greatest in V1
--There is also ST Elevation in lead III, and reciprocal ST depression in aVL
--There is ST depression in V5 and V6
One might suspect these findings to indicate an inferior and right ventricular infarct, but a (left ventricular) septal infarct with a wraparound LAD to the inferior wall will give the same pattern and is more likely, especially due to the bifascicular block.
Now the etiology of her entire clinical presentation (except fever) is obvious.
She arrested again before she could get to the cath lab. So no angiogram was done.
On arrival, medics found the patient with agonal respirations. Chest compressions were started and 2 doses of epinephrine givne, and she was found to be in asystole, which then changed to PEA at some point, then to ventricular tachycardia. A King airway was placed.
This is her prehospital ECG:
 |
| What do you think? My thoughts are below. |
On arrival, she was hypertensive and tachycardic. Due to concern for hyperkalemia, Calcium was given empirically. Cardiac ultrasound showed poor LV function and normal RV size. K returned at 5.8 mEq/L (not high enough to be responsible for all of this).
An ED ECG was obtained:
 |
| What do you think? |
ECGs:
Prehospital:
--There is sinus tachycardia.
--The large R-wave in V1, with wide S-wave in V5 and V6 shows late forces toward V1 and away from V5 and V6, and is therefore diagnostic of right bundle branch block (RBBB).
--The large inferior S-waves, with a small q- and large R-wave in aVL are diagnostic of left anterior fascicular block.
--(Bifascicular block, RBBB and LAFB).
--Importantly, the PR interval is normal. If prolonged, there would be so-called trifascicular block.
These findings alone are very suggestive of LAD or left main occlusion. Every such case I have ever encountered was in a patient with either left main occlusion or LAD occlusion and the patient was near death or post-arrest.
This is a very bad sign, and the ST Elevation in these cases is frequently very subtle.
Finally, there are very large (hyperacute) T-waves in II, III, aVF and in V4-V6. These are diagnostic of either hyperkalemia or of acute STEMI.
Here are some cases of STEMI with RBBB and LAFB
Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation
don't miss this one!
ED ECG:
--Sinus tachycardia with RBBB and LAFB
--There is subtle ST elevation in V2-V5
Here the precordial leads are magnified:
 |
| Notice that there is almost 2 mm ST Elevation in V2 2 mm ST elevation in V3 1 mm ST Elevation in V4 |
RBBB should not have ANY ST elevation, so this is STEMI until proven otherwise.
In fact, in leads with a prominent R'-wave (here, as is usual: V1-V3), there should be ST depression that is discordant to the prominent R'-wave)
Here is an example of RBBB without any ischemia:
 |
| Note normal (non-ischemic) ST depression in V1-V3, discordant to positive R'-wave |
The ST elevation was not seen.
She had fever and elevated lactate.
Sepsis and pulmonary embolism were suspected.
CT pulmonary angiogram was negative.
After this, she had another brady-asytolic arrest and was resuscitated again.
Another ECG was obtained:
 |
| Now the anterior STEMI is obvious (in addition to right bundle branch block and left anterior fascicular block) |
Further comment on this ECG:
--The ST elevation is greatest in V1
--There is also ST Elevation in lead III, and reciprocal ST depression in aVL
--There is ST depression in V5 and V6
Notice the RBBB with LAFB is gone! I cannot explain this except to say that any new bundle branch block in any situation can be transient.
One might suspect these findings to indicate an inferior and right ventricular infarct, but a (left ventricular) septal infarct with a wraparound LAD to the inferior wall will give the same pattern and is more likely, especially due to the bifascicular block.
Now the etiology of her entire clinical presentation (except fever) is obvious.
She arrested again before she could get to the cath lab. So no angiogram was done.
The ST segment elevation is bigger in v1 than v2
ReplyDeleteIt is tipical of Vd infarction
I think it is possible that the RCA was culprit vessel
That is very likely
DeleteThank you, as always for these cases. I read them as a priority. One question - would you usually do a CTPA for PE if you have a normal sized RV on early bedside ECHO? Is it still a matter where some teams are not trusting of the result, or is bedside ECHO an inadequate screen?
ReplyDeleteKylie,
DeleteGood question. I would not have obtained a CTPA. I think they are done too often. With good RV function on echo, and poor LV function, this is not going to be PE.
Steve Smith