A middle-aged male with a history of 2-vessel coronary bypass called 911 because of the relatively sudden onset of severe SOB. He had had more mild SOB for the past 2 days. The medics found him in respiratory distress with coarse breath sounds, a BP of 196/132, oxygen saturations of 90%, and a pulse of 130. They put him on CPAP for respiratory support. He denied chest pain.
Here is his prehospital ECG:
The patient arrived in the ED and was put on Noninvasive ventilation (BiPAP). Blood Pressure was 200/110. A nitroglycerin drip was started and this ECG was recorded:
Bedside echo showed diffuse B-lines of pulmonary edema.
The plan was to completely control the blood pressure and re-assess for ischemia.
BP was controlled to 120/70 with very high dose Nitro, and the patient's respiratory distress was improved, and another ECG was recorded:
Now we have controlled the excessive demand but the ischemia persists: the BP is not elevated, the heart rate is only mildly elevated, there is no more hypoxia, the hemoglobin returned normal, and there is no evidence of valvular dysfunction (at least no murmur).
Thus, ACS is very likely the initiating factor. So we have ACS with both refractory symptoms and pulmonary edema, both of which are indications for cath lab activation.
ST depression in the precordial leads can be either posterior STEMI or diffuse subendocardial ischemia. Does this matter? No! This is ACS that needs the cath lab now because it is refractory to medical management.
There are those who think this ECG pattern in ACS is due to left main occlusion. This is not accurate. See this exhaustive post on the topic.
The cath lab was activated.
Normally, a P2Y12 inhibitor (clopidogrel, ticagrelor) would be given, but in this case with STE in aVR and diffuse ST depression, there is high potential for left main insufficiency or severe 3 vessel disease. Thus, there was approximately a 50% likelihood that the patient would need CABG (surgical bypass), although this probability is less in a patient with previous bypass. Clopidogrel or even ticagrelor would increase the risk of severe bleeding at surgery.
Thus, eptifibatide was given instead of ticagrelor. Eptifibatide can be turned off.
The patient could not lie flat and so was intubated.
The patient went to the cath lab and had a 100% mid circumflex occlusion that was opened. Since bypass would not be needed, ticagrelor was initiated.
The outcome was good except for some bleeding complications, during which time his P2Y12 inhibitor (ticagrelor) needed to be held.
The echocardiogram confirmed a posterior wall motion abnormality. The troponin I peaked at 20 ng/mL.
Epilogue
The patient returned a few weeks later with the identical presentation: respiratory failure, pulmonary edema, and severe hypertension. His ECG is shown here:
After treatment with BiPAP and IV Nitroglycerin, his symptoms greatly improved and this ECG was recorded:
Because of the recent stent and the time off of clopidogrel, an angiogram was done and showed no in-stent thrombosis (no new ACS). The troponin peaked at 1.5 ng/mL and there was no new wall motion abnormality.
This ST Depression was due entirely to supply/demand mismatch, not due to ACS. The second presentation was purely a type II MI.
Learning Points:
1. In the setting of ischemia, before diagnosing ACS, manage the oxygen supply and demand issues first. Use supportive care. Then re-assess. If ischemia persists, then it is ACS.
2. If ACS and symptoms are refractory, it does not matter whether it is a posterior STEMI or diffuse subendocardial ischemia. Emergent angiogram and PCI if indicated should be undertaken.
Here is his prehospital ECG:
 |
| There is diffuse ST depression, with ST elevation in lead aVR |
The patient arrived in the ED and was put on Noninvasive ventilation (BiPAP). Blood Pressure was 200/110. A nitroglycerin drip was started and this ECG was recorded:
 |
| Same as prehospital The ischemia could be due to supply/demand ischemia from hypoxia, tachycardia, and hypertension, or it could have been initiated by ACS. The ECG cannot differentiate. If ACS, it could be diffuse subendocardial ischemia, or posterior STEMI. Does that matter? |
Bedside echo showed diffuse B-lines of pulmonary edema.
The plan was to completely control the blood pressure and re-assess for ischemia.
BP was controlled to 120/70 with very high dose Nitro, and the patient's respiratory distress was improved, and another ECG was recorded:
 |
| Continued ST depression |
Now we have controlled the excessive demand but the ischemia persists: the BP is not elevated, the heart rate is only mildly elevated, there is no more hypoxia, the hemoglobin returned normal, and there is no evidence of valvular dysfunction (at least no murmur).
Thus, ACS is very likely the initiating factor. So we have ACS with both refractory symptoms and pulmonary edema, both of which are indications for cath lab activation.
ST depression in the precordial leads can be either posterior STEMI or diffuse subendocardial ischemia. Does this matter? No! This is ACS that needs the cath lab now because it is refractory to medical management.
There are those who think this ECG pattern in ACS is due to left main occlusion. This is not accurate. See this exhaustive post on the topic.
The cath lab was activated.
Normally, a P2Y12 inhibitor (clopidogrel, ticagrelor) would be given, but in this case with STE in aVR and diffuse ST depression, there is high potential for left main insufficiency or severe 3 vessel disease. Thus, there was approximately a 50% likelihood that the patient would need CABG (surgical bypass), although this probability is less in a patient with previous bypass. Clopidogrel or even ticagrelor would increase the risk of severe bleeding at surgery.
Thus, eptifibatide was given instead of ticagrelor. Eptifibatide can be turned off.
The patient could not lie flat and so was intubated.
The patient went to the cath lab and had a 100% mid circumflex occlusion that was opened. Since bypass would not be needed, ticagrelor was initiated.
The outcome was good except for some bleeding complications, during which time his P2Y12 inhibitor (ticagrelor) needed to be held.
The echocardiogram confirmed a posterior wall motion abnormality. The troponin I peaked at 20 ng/mL.
Epilogue
The patient returned a few weeks later with the identical presentation: respiratory failure, pulmonary edema, and severe hypertension. His ECG is shown here:
 |
| There is diffuse ST depression and ST elevation in aVR, although not as profound as the first time |
After treatment with BiPAP and IV Nitroglycerin, his symptoms greatly improved and this ECG was recorded:
 |
| The supply/demand issues are gone and the ST depression is resolved. |
Because of the recent stent and the time off of clopidogrel, an angiogram was done and showed no in-stent thrombosis (no new ACS). The troponin peaked at 1.5 ng/mL and there was no new wall motion abnormality.
This ST Depression was due entirely to supply/demand mismatch, not due to ACS. The second presentation was purely a type II MI.
Learning Points:
1. In the setting of ischemia, before diagnosing ACS, manage the oxygen supply and demand issues first. Use supportive care. Then re-assess. If ischemia persists, then it is ACS.
2. If ACS and symptoms are refractory, it does not matter whether it is a posterior STEMI or diffuse subendocardial ischemia. Emergent angiogram and PCI if indicated should be undertaken.
dr.smith
ReplyDeletevery nice case to learn from . what is the difference between LM Insufficiency and LM occlusion .i read some where that if ST lelevation in AvR > V1 then would be LM OCCLUSION .what do think?
khalid
No! Read the last section of this paper I wrote:
Deletehttp://www.researchgate.net/publication/257809517_Updates_on_the_Electrocardiogram_in_Acute_Coronary_Syndromes
Hi, u started with "A middle-aged male with a history of 2-vessel coronary bypass ". What was this 2vessels? It may not be grafted vessel stenosis/occlusion? Thank you
ReplyDeleteThey were grafts to the LAD and to a small posterolateral branch off the circumflex
DeleteInteresting case, with same presentation of two differents pathologies. I´m curious about one item in this case. In your place of work use a GIIB/IIIA inhibitor instead of a P2Y12 inhibitor without a cardiologist or hemodinamist advice?
ReplyDeleteThanks for the feedback.
I don't recommend it without cardiologist input. In this case, the cardiologist did not like it and stopped it. Then when he did the cath, he started it again. So it was the right decision, but it is always a tough one and may be controversial.
DeleteGREAT case! I would not have predicted a mid-circumflex lesion from the initial 3 ECGs, as the ST depression was more diffuse that what I’d typically expect for posterior MI. But as you explain — it was a mid (presumably dominant) left circumflex occlusion with posterior wall motion abnormality confirmed on Echo … so quite educational to read your explanation.
ReplyDeleteOtherwise — I like to point out the T wave peaking (esp. well seen in the last ECG after resolution of the ST depression) may be a manifestation of ischemia.
THANKS for presenting!
Ken
DeleteGood points, thanks!
Steve
Great case. I have two comments 1) Being that this was a true occlusion (100%), looking back this was STEMI. Would the patient not have benefited from emergent cath up front instead of taking time for labs medical treatment etc? Time is myocardium?
ReplyDelete2) Second question is treating to reverse the signs of the chest pain and ischemic ekg is great, but there are a number of posts declaring the dynamic nature of ACS and although the ischemia or even STEMI on ekg resolves these patients can be high risk and re-occlude at any time. STEMI or stemi-equivalent ekg that improves should still go emergently to cath no? Thanks for your help in advance.
Yes, NonSTEMI can occlude at any time. thrombus can propagate. That's why I advocate for aggressive medical care and insist the both symptoms and EKG findings resolve and that the patient have continuous 12-lead monitoring. I have never had an undetected occlusion in these cases. There is no evidence that they have to have emergent intervention.
DeleteAs I point out in the article, the majority of such patients do not even have ACS. They have other illness that creates supply demand ischemia in the setting of fixed coronary disease. Intervention is unequivocally harmful in these patients.
It is a default of paramedics and EPs that somehow intervention is a magical therapy and good for everyone. It needs to be carefully applied.
In fact, if a patient has a spontaneously reperfused STEMI, it is also a high risk situation and I have always advocated emergent intervention in these patients. however, I would not be surprised if even those patients could be treated with aggressive medical therapy and continuous 12-lead ST segment monitoring.
Steve Smith
Just a comment that we can't look back and say this was a STEMI. An occluded artery does NOT always mean STEMI, which implies transmural infarction. If you have a lot of collateral circulation to perfuse around the obstruction like this man, it may not lead to ST elevation on the ECG. In his case, as Dr. Smith mentions, he may have had a posterior STEMI, and regardless of the ECG findings he needed emergency catheterization as he was refractory to medical therapy.
DeleteBut in this case you can say it was a STEMI. The ST depression caused by the LCx as the culprit can only be reciprocal to ST elevation of the posterior wall, also confirmed by echo. The second time it was not due to ACS, and was indeed subendocardial ischemia.
DeleteThanks for the response. Appreciate your input and advice.
ReplyDeletethamks steve....yesterday in clinic i came across with exactly same ECG changes. on echo inferoposterior wall hypokinesia, referred to ER.Cath lab was not available ,
ReplyDeletethrombolytic therapy given/ unfortunately she couldnot survive
my question is .....in your mentioned case scenario if cath lab is not available, what are the most specific ECG changes to diagnose as posterior wall MI to give thrombolytic therapy
ReplyDeleteIf you have no Cath lab, thrombolytic therapy can be given in either situation. The new 2013 STEMI guidelines finally approve diffuse ST depression, with ST elevation in aVR (due to ACS) as an indication for thrombolytic therapy!
DeleteSteve Smith
if the culprit lesion was LCX and this was just post STEMI, then what is the expalanatinon of STE in aVR?
ReplyDeleteAny time there is ST depression in V5 and II, there will be STE in aVR. STE in aVR is not 100% specific to LM or 3 vessel ischemia. It is sometimes present in posterior STEMI.
Delete