ECG sagas of subtlety 2
You may have noticed that I am an ECG geek – I love their simplicity and their complexity. I certainly don’t claim guru status, as I don’t possess expertise in the same way that Amal Mattu or Steve Smith do, but I do love ECGs.
I regularly arrive on the ED floor at morning handover, and go ECG-snooping. When I hear a handover mentioning chest pain in any shape or form and the phrase “but the ECG was OK/normal/no acute changes”…etc, I complete the handover, and go and review the ECGs myself. No doubt, the residents hate me for it.
For this reason I regularly unearth “missed” abnormal and instructive ECGs which could be considered subtle (although worryingly sometimes they are barn-door obvious) and hence the “ECG sagas of subtlety” series was born in an attempt to share the lessons learned. I don’t intend criticism of the doctors involved. These are often subtle and difficult ECG findings. The one I share here was discovered on one such snoop:
The case: Chronologically a 50 year old man with 70 year old physiology, who presented with central chest and back pain. He was centrally obese, a diabetic, and had a history of prior warfarinisation for DVT, recently ceased.
This is his time-zero ECG (apologies for reproduction quality, but click on it and it should be discernable):
with chest and back pain at time zero
The night crew spotted the ST depression in III and aVF, called it “ischaemia” and treated the patient as ACS. I came on in the morning, heard the story and heard that the ECG was “OK,” and went snooping.
WHEN YOU SEE ST DEPRESSION YOU SHOULD ALWAYS LOOK FOR THE ST ELEVATION THAT IT MAY BE RECIPROCAL TO
Unfortunately this went unrecognised. The patient was given 300mg of aspirin and 2 sprays of GTN. He had some improvement in his anterior chest pain, however his back pain was more severe than the chest pain and was ongoing. The following ECG was recorded 2 hours later in the context of ongoing pain: with ongoing back pain
I met this man about 2 hours after this second ECG, four hours into his presentation. He had ongoing back pain and looked uncomfortable. He was given further antiplatelet therapy and anticoagulated, then referred to cardiology. His troponin peaked at 3.5. This man had a “missed” high lateral STEMI. Did missing this have adverse consquences? Hard to know really. We may have saved a bit more myocardium if he’d gotten to PCI earlier. There were further delays to PCI and the case was somewhat frustrating. If you are interested in reading further on high lateral STEMI, click on this link to the always enlightening Steve Smith’s take on the topic. To quote Steve: “When there is inferior ST depression, one is tempted to diagnose “inferior ischemia”. However (paradoxically and mysteriously) there is no correlation between location of subendocardial ischemia on the ECG and the location of the ischemia in the heart. When there is subendocardial ischemia, the ST depression tends to be diffuse. So what does “inferior” ST depression represent? It is reciprocal to high (lateral) ST elevation until proven otherwise“
And there you have it. His discharge letter from the treating team is still calling this an NSTEMI. For me, it is a STEMI with the D1 vessel being the culprit lesion that correlates nicely with the ECG changes
I’m right on board with you. There’s also horizontal ST-depression from V1-V3 with a tall T-wave in V2, so I’m calling it a subtle postero-lateral STEMI. Definitely a candidate for reperfusion, especially with the incomplete response to medical therapy.
Nice catch! I’m glad I’m not the only one who goes snooping around for these “but the ECG was normal…” cases at the start of every shift. It’s stated that the LCX is often electrically silent, and I’m sure it sometimes is, but very often you just need to know what to listen for…
Was trying to respond to your other comment and deleted it – big fingers, small screen iPhone. Can you re-post? I had neglected to point out the tall R wave in V2/3 in original post
By “tall T-wave in V2″ I meant “tall R-wave.” My bad. Thanks for sharing the great case, we can never have too many of these.
There is a slight ST-segment elevation in leads I and aVL suggesting, but not diagnostic of, a diagonal artery occlusion. The next step, of course, is to repeat the ECG and look for changes. The diagonal vessel in this case may be a D1, D2 or a ramus intermedius vessel that affects the lateral wall, but not necessarily the obtuse margin. -Wayne
ECG at time 0 shows
1) sinus rhythm with each QRS complexes preceded by P waves. P waves are seen upright in most limb leads suggesting its sinus origin
2) P waves morphology bifid in appearance, P mitrale, suggesting left atrial enlargement
3) axis normal
4) QRS complexes narrow, regular with no RR variation, beating at a rate of approximately 60 beats per minute
5) subtle but significant 1mm concave upwards ST elevation seen in the high lateral leads, lead Iand aVL. Q wave also noted in lead I
6) this is coupled by reciprocal changes over the inferior leads. Significant horizontal ST segment depression seen in lead II,III and aVF.
7) horizontal ST segment depression were also seen over lead V2 to V4 with a tall R wave seen in V2 with R/S ratio more than 1
Impression: evolving posterolateral STEMI. Culprit artery likely to be left circumflex. Urgent reperfusion via PCI indicated
The denouement is of course the cath result:
■diffuse CAD
■obstruction of 1st LAD diagonal branch
■anterior wall hypokinesis, mild-mod LV dysfunction
And there you have it. His discharge letter from the treating team is still calling this an NSTEMI. For me, it is a STEMI with the D1 vessel being the culprit lesion that correlates nicely with the ECG changes
Nice ECG and analysis.
Just as a usual-practice / protocol issue, though… and at the risk of retrospectoscoping the night crew, if the working diagnosis was NSTEACS, even if the cath. lab wasn’t activated (as it wasn’t viewed as a STEMI-equivalent), wouldn’t you normally give a LMWH (or just heparin) in addition to an antiplatelet agent (perhaps something in addition to aspirin, too) particularly in the context of ongoing pain?
Yes….although this is a bit like the heparin in VTE debate, in that the actual benefit has never been proven, and the indication remains somewhat unclear, based on old MI classifications that no longer are used… See the NNT.com for more: http://www.thennt.com/nnt/heparin-for-acute-coronary-syndromes/
Very true. I’m afraid I still allow myself to suffer somewhat from the inertia of still being held intellectual hostage by the cardiology service at my usual hospital for whom the rate of change of practice based on best evidence might most generously be described as… glacial.