A 30-something presented with methamphetamine use and agitation. He was sedated, then had an ECG as part of his workup:
He was stabilized and observed.
He was still confused 8 hours later when I was now on duty, and he was found to have a heart rate of 140, so another ECG was recorded:
I suspected some lead misplacement and ordered another with the leads corrected:
What do you think? This is what I thought:
First, whenever I see ST elevation in the setting of severe tachycardia, I am very skeptical of STEMI. STEMI is only associated with tachycardia when there is 1) cardiogenic shock or 2) another simultaneous pathology.
Second, the ST Elevation just does not look like the STE of anterior STEMI. How do I explain? I'm not sure. All I can do is show you as many ECGs as possible until you see the difference. For me, it is like recognizing a face (or not). This is not the face of anterior STEMI.
Third. Of course you must always be vigilant and realize that you can mis-recognize a face, especially if you don't have my experience. ("Sorry I didn't recognize you! I thought you were my friend PseudoSTEMI.....")
With this blog, I'm trying to help you get that extra experience, and to recognize these patterns.
What do you want to do? Go see the patient, of course.
The patient was agitated and confused and able to say that he did not have chest pain, but did have a sore throat (important: he can feel pain). His throat was very erythematous (the throat pain was NOT due to MI, as is sometimes the case).
He was clearly NOT in cardiogenic shock. He felt hot and so I measured an oral temp (102.2 F = 38.5 C) and then a rectal temp (104.9 F = 40.5 C). We did a point of care ultrasound which showed hyperdynamic function and all walls clearly contracting normally.
We treated him for hyperthermia (acetaminophen and cool mist) and infection, gave fluids, antibiotics, and high dose benzodiazpines (lorazepam). He needed to be intubated for altered mental status and agitation. He had a negative head CT and lumbar puncture.
His heart rate slowly came down to 129.
Another ECG was recorded:
He was admitted to the ICU.
He was found to have clonus later that night, all but diagnostic of serotonin syndrome (for which he had already been appropriately treated). A comprehensive drug screen (ours routinely uses extremely sensitive mass spectrometry on all cases) confirmed amphetamine and methamphetamine, both of which can cause serotonin syndrome.
All troponins overnight were below the level of detection.
An ECG was recorded the next morning:
Whether there is or is not type 2 Brugada is uncertain. Strictly speaking, this appears to meet the criteria. But as the posts below demonstrate, type 2 Brugada is pretty vague and its significance uncertain and probably exaggerated.
Why does tachycardia lead to such ST Elevation, and how did you know it was not a STEMI?
I don't know why this happens. I've just seen a lot of it and recognized it as NOT a STEMI.
Perhaps a type 2 Brugada at baseline, in combination with serotonin syndrome, resulted in ST elevation?
Learning Point:
See above. When there is severe tachycardia, STE is unlikely to be STEMI unless there is cardiogenic shock. Assess the whole patient, do a full evaluation, get the heart rate down, then re-evaluate the ECG findings. Do a high quality cardiac ultrasound.
Criteria for Type 2 Brugada syndrome
See these posts:
For an important update on this post, go here:
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. 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. The base of the triangle outlined should be longer than 3.5 mm. This confirms that the slope of the ST segment is flat enough for the diagnosis. I explain this in an annotated version here:
He was stabilized and observed.
He was still confused 8 hours later when I was now on duty, and he was found to have a heart rate of 140, so another ECG was recorded:
 |
| There is one lead (V2) with massive ST elevation. Since there is very little STE in V1 or V3, there must be lead misplacement. |
I suspected some lead misplacement and ordered another with the leads corrected:
 |
| Now there is massive STE in BOTH leads V2 and V3 What do you think? What do you want to do? |
What do you think? This is what I thought:
First, whenever I see ST elevation in the setting of severe tachycardia, I am very skeptical of STEMI. STEMI is only associated with tachycardia when there is 1) cardiogenic shock or 2) another simultaneous pathology.
Second, the ST Elevation just does not look like the STE of anterior STEMI. How do I explain? I'm not sure. All I can do is show you as many ECGs as possible until you see the difference. For me, it is like recognizing a face (or not). This is not the face of anterior STEMI.
Third. Of course you must always be vigilant and realize that you can mis-recognize a face, especially if you don't have my experience. ("Sorry I didn't recognize you! I thought you were my friend PseudoSTEMI.....")
With this blog, I'm trying to help you get that extra experience, and to recognize these patterns.
What do you want to do? Go see the patient, of course.
The patient was agitated and confused and able to say that he did not have chest pain, but did have a sore throat (important: he can feel pain). His throat was very erythematous (the throat pain was NOT due to MI, as is sometimes the case).
He was clearly NOT in cardiogenic shock. He felt hot and so I measured an oral temp (102.2 F = 38.5 C) and then a rectal temp (104.9 F = 40.5 C). We did a point of care ultrasound which showed hyperdynamic function and all walls clearly contracting normally.
We treated him for hyperthermia (acetaminophen and cool mist) and infection, gave fluids, antibiotics, and high dose benzodiazpines (lorazepam). He needed to be intubated for altered mental status and agitation. He had a negative head CT and lumbar puncture.
His heart rate slowly came down to 129.
Another ECG was recorded:
 |
| Almost all ST Elevation is resolved |
He was admitted to the ICU.
He was found to have clonus later that night, all but diagnostic of serotonin syndrome (for which he had already been appropriately treated). A comprehensive drug screen (ours routinely uses extremely sensitive mass spectrometry on all cases) confirmed amphetamine and methamphetamine, both of which can cause serotonin syndrome.
All troponins overnight were below the level of detection.
An ECG was recorded the next morning:
 |
| This is suggestive of Type 2 Brugada syndrome (see criteria below). |
Whether there is or is not type 2 Brugada is uncertain. Strictly speaking, this appears to meet the criteria. But as the posts below demonstrate, type 2 Brugada is pretty vague and its significance uncertain and probably exaggerated.
Why does tachycardia lead to such ST Elevation, and how did you know it was not a STEMI?
I don't know why this happens. I've just seen a lot of it and recognized it as NOT a STEMI.
Perhaps a type 2 Brugada at baseline, in combination with serotonin syndrome, resulted in ST elevation?
Learning Point:
See above. When there is severe tachycardia, STE is unlikely to be STEMI unless there is cardiogenic shock. Assess the whole patient, do a full evaluation, get the heart rate down, then re-evaluate the ECG findings. Do a high quality cardiac ultrasound.
Criteria for Type 2 Brugada syndrome
See these posts:
Is this Type 2 Brugada syndrome/ECG pattern?
Non-Vagal Syncope and Saddleback Morphology in V2
This is a post showing the difficulty of the decision to place an implanted defibrillator.
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. 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. The base of the triangle outlined should be longer than 3.5 mm. This confirms that the slope of the ST segment is flat enough for the diagnosis. I explain this in an annotated version here:
 |
| Explanation 1. Draw a horizontal line from top of r' wave (black line 1) 2. Draw a horizontal line 5 mm below this (green line 2) 3. Extend the downsloping r'-ST segment (black line 3) until it intersects the green line 4. Measure the base. If greater than 3.5 mm, then meets criteria (this is equivalent to a 35 degree beta angle) |
Brilliant as usual
ReplyDeleteGlad you liked it. Thanks.
DeleteExcellent.
ReplyDeleteMaybe, this case we can be another case of brugada phenocope.
Look this article : Daniel D Anselm, Jennifer M Evans, Adrian Baranchuk : Brugada phenocopy: A new electrocardiogram phenomenon World J Cardiol 2014 March 26; 6(3): 81-86.
"Since the initial reports, type 1 Brugada phenocopy have been reported in the context of an acute inferior ST-segment elevation myocardial infarction with right ventricular involvement ; concurrent hyperkalemia, hyponatremia and acidosis ; acute pulmonary embolism; and hypokalemia in the context of congenital hypokalemic periodic paralysis .
Type 2 Brugada phenocopy have been reported immediately post-electrocution accidental injury; in the context of congenital pectus excavatum causing mechanical mediastinal compression ; and as a result of an inappropriate high-pass ECG filter
Brugada phenocopies are clinical entities that present with an ECG pattern identical to either the type 1 or type 2 Brugada patterns yet differ etiologically from true Brugada syndrome. The pattern presents in association with an identifiable condition and, upon resolution of that condition, the ECG pattern normalizes"
Thanks for this. Excellent points about the tachycardia and patient assessment!
ReplyDelete