A middle-aged woman had sudden pulmonary edema in the middle of the night. There was no known history of left bundle branch block. There was no chest pain.
Her blood pressure was 200/110. Here was her initial ED ECG:
In our study of occlusion in STEMI, we excluded patients with tachycardia or pulmonary edema because they often have false positive ST elevation (tachycardia exaggerates the discordant ST elevation and depression of LBBB). They do not commonly have false negative ST elevation. I would be very surprised if a patient with this ECG had active persistent LAD occlusion, though as with any ECG, circumflex occlusion can easily be missed.
A bedside echo was done by a highly skilled ED Echo expert. Here is the parasternal long axis view:
He then performed a parasternal short axis view:
This appears to show an anteroseptal wall motion abnormality.
Images were done with speckle tracking, but unfortunately could not be uploaded. Here are some images of ultrasound speckle tracking from another case of LBBB.
However, LBBB affects the sequence of activation of the ventricle (dyssynchrony) which appears to the interpreter as a wall motion abnormality. Is this just dyssynchrony, or is there a wall motion abnormality?
Chest X-ray and sonographic B-lines confirmed pulmonary edema.
The patient was put on BiPAP and high dose nitroglycerine.
The cardiologist was consulted for possible cath lab activation and was certain this was not acute coronary occlusion. The cath lab was not activated.
The patient was able to be weaned from BiPAP in the ED. A repeat ECG was obtained:
Was this a brief occlusion of the LAD that was invisible on the ECG, and only showed up as a wall motion abnormality?
A Formal Echocardiogram was done:
Decreased left ventricular systolic performance severe .
Left ventricular hypertrophy concentric borderline.
Regional wall motion abnormality-mid anterior wall with sparing of apex.
(Our ED echo expert was correct). But the ECG was even more correct.
Troponin I Peaked at 0.054 (0.030 is 99%).
Thus, a non-emergent angiogram was done:
Angiogram: Normal coronary arteries. (No plaque at all.)
Final diagnosis: Idiopathic cardiomyopathy. Etiology of WMA unknown. No MRI done for assessment of other etiologies.
Learning points:
1. In acute pulmonary edema, if the ECG does not show ischemia, and there is another etiology (severe hypertension), and the pulmonary edema resolves with supportive care and NTG, then it is unlikely to require emergent angiogram for severe ACS.
2. New LBBB by itself, without any concordance or excessive discordance, is of little value in diagnosing acute STEMI or severe ischemia.
Her blood pressure was 200/110. Here was her initial ED ECG:
 |
| Sinus Tachycardia with Left Bundle Branch Block. There is no concordant ST elevation. There is no proportionally excessively discordant ST elevation. The highest ST/S ratio is in V1 at 2.5/27 = 0.093 (normal). There is no evidence of ischemia on this ECG, and certainly no evidence of STEMI |
In our study of occlusion in STEMI, we excluded patients with tachycardia or pulmonary edema because they often have false positive ST elevation (tachycardia exaggerates the discordant ST elevation and depression of LBBB). They do not commonly have false negative ST elevation. I would be very surprised if a patient with this ECG had active persistent LAD occlusion, though as with any ECG, circumflex occlusion can easily be missed.
A bedside echo was done by a highly skilled ED Echo expert. Here is the parasternal long axis view:
He then performed a parasternal short axis view:
This appears to show an anteroseptal wall motion abnormality.
Images were done with speckle tracking, but unfortunately could not be uploaded. Here are some images of ultrasound speckle tracking from another case of LBBB.
However, LBBB affects the sequence of activation of the ventricle (dyssynchrony) which appears to the interpreter as a wall motion abnormality. Is this just dyssynchrony, or is there a wall motion abnormality?
Chest X-ray and sonographic B-lines confirmed pulmonary edema.
The patient was put on BiPAP and high dose nitroglycerine.
The cardiologist was consulted for possible cath lab activation and was certain this was not acute coronary occlusion. The cath lab was not activated.
The patient was able to be weaned from BiPAP in the ED. A repeat ECG was obtained:
 |
| Slower rate, even less ST elevation (expected, as discordant STE in LBBB is exaggerated by tachycardia) |
Was this a brief occlusion of the LAD that was invisible on the ECG, and only showed up as a wall motion abnormality?
A Formal Echocardiogram was done:
Decreased left ventricular systolic performance severe .
Left ventricular hypertrophy concentric borderline.
Regional wall motion abnormality-mid anterior wall with sparing of apex.
(Our ED echo expert was correct). But the ECG was even more correct.
Troponin I Peaked at 0.054 (0.030 is 99%).
Thus, a non-emergent angiogram was done:
Angiogram: Normal coronary arteries. (No plaque at all.)
Final diagnosis: Idiopathic cardiomyopathy. Etiology of WMA unknown. No MRI done for assessment of other etiologies.
Learning points:
1. In acute pulmonary edema, if the ECG does not show ischemia, and there is another etiology (severe hypertension), and the pulmonary edema resolves with supportive care and NTG, then it is unlikely to require emergent angiogram for severe ACS.
2. New LBBB by itself, without any concordance or excessive discordance, is of little value in diagnosing acute STEMI or severe ischemia.
Dilated cardiomyopathy? Does one not need to be careful with nitro administration with that presentation?
ReplyDeleteNot when there is plenty of blood pressure. Nitro is essential. And it was exactly what made the patient better.
DeleteNICE case - and great as always that you include Echos and clinical follow-up going step-by-step with what happened in the ED! As to the question by Anonymous - I'd add the beauty of giving NTG IV is that you have moment-to-moment titrability - so as you say, this was the medication that made the patient better!
ReplyDeleteOtherwise - I initially thought there might be a little extra peaking in the T waves on the original ECG in the inferior leads and in V5 - but as you mentioned, with the 2nd ECG that showed slowing of the rate - this did not evolve. GREAT explanation - THANKS for posting! - : )
T wave is upright in lead II while QRS is positive, isnt that weird ? great explanation as said Ken Grauer.
ReplyDeleteYes. a Bit. But not terribly unusual.
DeleteVery weird. The echo clearly shows akinesia of the entire septum. In dyskinesia from LBBB the septum has a delayed contraction, which might look like hypokinesia, but here it just doesn't move at all.
ReplyDeleteAan,
DeleteYes. No good explanation. But the ECG was right and the echo was wrong!
Steve