I was working a busy shift in the ED, like many of us do, and the next patient I was going to see was a 57 year old male with no real medical problems complaining of chest pain. I remember thinking as I walked into the room this guy looks ashen and diaphoretic….he doesn’t look well. He is a paramedic telling me how he has been having off and on chest pain for the past several months. He just had a stress test two months ago that was “negative”. Today he was working on his pool and developed the same chest discomfort as he had been having off and on the past several months, but today, the pain would just not go away. In his mind, he thought this might be an ulcer and just needed some Pepcid to help. He got put on the monitor and an ECG was run…
The patient involved in this case has given permission to share the story, and relevant images with the knowledge that this information will be used for the purposes of education.
This was read by the ECG machine as normal sinus rhythm and age undetermined septal infarct. Looking closer at leads V2 and V3 I can imagine that I am seeing some ST-segment elevation. Given he was diaphoretic, I was thinking this was an evolving anterior STEMI. So I asked for a second ECG and quickly ran to get the ultrasound machine so I could do a bedside POCUS to look for wall motion abnormalities. The 2nd ECG was done, but I didn’t get to see it until much later, as a Code Blue was called overhead. Here is the 2nd ECG by the way…
Again the ECG machine read this as normal sinus rhythm with age undetermined septal infarct, but as you can clearly see there is more ST-segment elevations in leads V2 and V3 when compared to the 1stECG. This is still not an anterior STEMI by definition (no mm criteria met), but it is diagnostic of a coronary occlusion.
I ran back to the room and saw a cyanotic patient, unresponsive getting CPR. The crash cart was called for and as we were waiting for the crash cart, the patient was intubated without difficulty. Defibrillation pads were placed on the patient and after one round of CPR (≈2minutes), ventricular fibrillation was seen on the monitor. The patient was successfully defibrillated with 200J on a biphasic machine…There was asystole on the monitor for about 5 – 10 seconds and then sinus tachycardia with ROSC.
It’s hard to have a great concept of time, but going back and reviewing the chart, all of this transpired within 10 minutes of the patients arrival to the ED. I finally did get to do the Post-ROSC POCUS at the bedside and sure enough the patient had an antero-septal wall motion abnormality. Lucky for both of us, cardiology happened to be in the department and saw the bedside POCUS. The patient was quickly taken to the cath lab and found to have a 100% proximal LAD lesion (“The Widow Maker”). He ended up getting 2 stents.
I went to follow up with the patient the next day and he is doing quite well. Extubated in <24hours, neurologically intact, and his cath showed an EF of 40 – 45%, a bit lower than I would like (But that’s ok, as he is alive and well for his three daughters and wife). As with anything we do in life and/or medicine, it is important to reflect on such cases as this, to see how we can improve ourselves and our care. There were three teaching points for me with this case, and I am sure I could come up with many more, oh and I also asked Stephen Smith of Dr. Smith’s ECG Blog to give me some expert peer review as well:
Teaching Point #1: Uselessness of “Negative” Stress Tests
Many emergency providers have taken care of patients with true acute coronary syndrome or even primary cardiac arrest despite having had a recent “negative” stress test. I know I have. Overreliance on “negative” stress tests can be a common reason for misdiagnosis or delays in patient care. It is important to remember that coronary artery disease can arise from atherosclerotic lesions that are only mildly stenotic with unstable plaques that rupture and not picked up by standard stress testing. There is a huge misconception about “negative” stress tests in the health care industry and by laypersons. The sensitivities and specificities for stress testing are often reported between 65 – 90% depending on which study you read. Here are two trials that stress this exact fact:
Trial #1 : This was a retrospective chart review of 164 patients with either a “negative” stress test (122 patients) or a “normal” indeterminate stress test (42 patients) over the past 3 years. 34 patients (20.7%) from the total cohort were determined to have significant coronary artery disease in the next 30 days. Significant coronary artery disease was defined as myocardial infarction identified by positive cardiac markers, subsequent positive stress test of any type, cardiac catheterization requiring intervention, CABG, or death due to medical cardiac arrest. Here is the troubling part…8/34 (23.5%) had their most recent stress test within 1 month prior to admission 7/34 (20.6%) had their stress test between 1 – 3 months, and 11/34 (32.4%) had their stress test between 6mo – 1 year. Of the total cohort of 164 patients, 13 patients (7.9%) had an AMI.
Trial #2 : This was a prospective evaluation of 186 patients who had been referred for coronary angiography for suspected stable angina. All patients had a normal ECG at rest, none had undergone coronary revascularization, or have diabetes mellitus. 50% of women and 25% of men who had reversible perfusion defects on coronary angiography had completely normal exercise electrocardiographic findings.
Teaching Point #1 Bottom Line: Stress testing is used to identify critical stenosis causing obstruction to coronary blood flow, however in the setting of acute myocardial infarction the underlying pathophysiology is plaque rupture and thrombus formation. Coronary lesions may not have been significant enough to be detected on stress testing. Therefore a prior “negative” stress test should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test.
Teaching Point #2: Use POCUS (or as I like to call it Stethoscope 2.0)
For obvious reasons I was not able to get a live recording of this patient’s bedside ultrasound, but thought it would be useful to put up some images and videos describing ultrasound and coronary anatomy as this clenched the diagnosis. So first, let’s start with an ECG and the coronary anatomy and then move on to echo and coronary anatomy.
Image from Marwick TH et al 
Apical 4 Chamber View – Thanks to Ben Smith (Checkout his Amazing Blog: Ultrasound of the Week)
Parasternal Long Axis – Thanks Again to Ben Smith (Twitter: @UltrasoundJelly)
Parasternal Short Axis – Thanks to Ben Smith
Teaching Point #2 Bottom Line: Use POCUS liberally, as this will save patients’ lives. I have started putting an ultrasound machine right next to me when I am on shift. When I go to evaluate patients I am ultra sounding as many hearts and lungs as I can. I cannot even begin to tell you the number of times, this has changed my disposition or expedited the care my patients received, including the above patient getting to the cath lab.
Teaching Point #3: Steve Smiths Early Repolarization vs “Subtle” Anterior STEMI Equation
Steve Smith over at Dr Smith’s ECG Blog has created a calculation that differentiates early repolarization vs subtle anterior STEMI. The key is the ratio of the T-wave amplitude to the R-wave amplitude. In anterior STEMI, the R-wave amplitude is smaller and early repolarization has a shorter QT interval. One HUGE CAVEAT, is that this equation should not be used in patients with LVH or LV aneurysms as this can cause false positives.
The Calculation: (1.196 x [ST-segment elevation 60ms after the J point in lead V3 in mm]) + (0.059 x [QTc in ms]) + (0.326 x [R-wave amplitude in lead V4 in mm)
Don’t worry, you don’t have to memorize this. It’s now on MD Calc
The Evidence : A retrospective study of patients with “subtle” (non-obvious) anterior STEMI and early repolarization at 2 hospitals had ECGs compared. 355 anterior STEMIs were reviewed and 143 of them were non-obvious and compared with 171 early repolarization ECGs. The generalized findings were: in “subtle” anterior STEMI the R-wave amplitude was lower in leads V2 – V4 and the QTc was longer when compared to early repolarization. Also a value of >23.4 predicted STEMI while a value of ≤23.4 was predictive of early repolarization. The overall sensitivity, specificity, and accuracy of this equation was 86%, 91%, and 88% respectively. This had a positive likelihood ratio of 9.2 and negative likelihood ratio of 0.1.
Getting ECG Nerdy:
60 Milliseconds (= 1.5 small boxes) after the J Point in V3
QTc not shown in ECG #1 above was 416ms
R Wave Amplitude in V4
So for the above patient…
(1.196 x [ST-segment elevation 60ms after the J point in lead V3 in mm]) + (0.059 x [QTc in ms]) + (0.326 x [R-wave amplitude in lead V4 in mm)
(1.196 x [2.7mm) + (0.059 x [416ms]) + (0.326 x [4.5mm]) = 26.3 which is suggestive of an anterior STEMI, not early repolarization
Teaching Point #3 Bottom Line: When you are having difficulty differentiating between benign early repolarization vs “subtle” anterior STEMI don’t forget about the Steve Smith equation to help differentiate between the two in the correct clinical setting.
Clinical Bottom Line & Things I Learned from the Case:
- A prior “negative” stress test, even if recently done, should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test.
- In patients having chest pain, use POCUS liberally, as this will save patients’ lives
- If you are having difficulty differentiating between benign early repolarization vs “subtle” anterior STEMI don’t forget about the Steve Smith equation to help differentiate between the two in the correct clinical setting
Expert Peer Review
I can see the ECGs better now, and also see the computer read. There is a Q-wave in lead V2. Since normal variant ST elevation never has Q-waves in V2 – V4, it must be assumed to be LAD occlusion (OMI – Occlusion Myocardial Infarction) even without using the formula. One might think this… there is a QS-wave in V2, therefore this is old MI. And the computer read is “age undetermined septal infarct.” But I have a rule for Old MI with persistent ST elevation (LV aneurysm morphology). The rule is based on the fact that acute MI has large T-waves compared to the QRS, and old MI has small T-waves.
ECG Differential May Include: Old anterior MI with Persistent ST Elevation (LV aneurysm morphology)
My rule for differentiating acute STEMI from LV aneurysm really only reliably distinguishes between:
- Acute STEMI on the one hand
- Subacute STEMI or LV aneurysm on the other
What is the Rule?
- First, there must be ST Elevation
- Second, the ECG differential diagnosis must be LV aneurysm (old MI with persistent ST Elevation) vs acute STEMI
- This rule should not be used for early repol vs acute STEMI. Conversely, if the differential is LV aneurysm vs acute STEMI, then you should NOT use the early repol formula
When should LV Aneurysm be on the ECG differential diagnosis?
Primarily when there are well-formed Q-waves, with at least one QS-wave, in V1 – V4. A QS-wave is defined by absence of any R-wave or r-wave of at least 1mm. (If there is an R-wave or r-wave, we call the whole wave a QR-wave, Qr-wave, or qR-wave, depending on the relative size of the Q-wave vs. R-wave.)
The Rule: If there is one lead of V1 – V4 in which the T/QRS ratio is greater than 0.36, then acute STEMI is the likely diagnosis, though subacute STEMI is also possible. Since both require the cath lab, if the ratio is greater than 0.36, and the clinical situation is right (i.e. unexplained chest discomfort), then cath lab activation is indicated. I both derived and validated this formula, for which the cutoff has good sensitivity and specificity.
- Derivation:Accuracy of Formula = 93.2% (Smith SW T/QRS Ratio Best distinguishes Ventricular Aneurysm from Anterior Myocardial Infarction. Am J Emerg Med 2005. PMID: 15915398)
- Validation:Sensitivity 91%, Specificity 81% (Electrocardiographic criteria to differentiate acute anterior ST-Elevation Myocardial Infarction from Left Ventricular Aneurysm. Am J Emerg Med 2015. PMID: 25862248)
- False negatives had pain duration greater than 6 hours.Thus, it may classify those patients with prolonged chest pain as LV aneurysm when they are really subacute STEMI.
Here is More Data on Stress Tests:
- Nerenberg et al. Impact of a Negative Prior Stress Test on Emergency Physician Disposition Decision in ED Patients with Chest Pain Syndromes. Am J Emerg Med 2007. PMID: 17157680
- Smith SW et al. Incidence of Myocardial Infarction in Emergency Department Chest Pain Patients with a Recent Negative Stress Imaging Test. Acad Emerg Med 2005.; 12:51 [Abstract]
- There were about 600 visits in 300 patients who had a negative stress imaging test within 3 years. There were 20 MIs, most in patients whose negative stress had been within the last year. We show that a recent negative stress imaging test is poor evidence that someone who returns to the ED with chest pain is not having an MI.
- Walker J et al. coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
- Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
- Marwick TH et al. Techniques for Comprehensive Two Dimensional Echocardiographic Assessment of left Ventricular Systolic Function. Heart 2003. PMID: 14594869
- Smith SW et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment elevation Myocardial Infarction. Ann Emerg Med 2012. PMID: 22520989
For More on this Topic Checkout:
- Smith’s ECG Blog: Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD Occlusion
- Smith’s ECG Blog: 12 Cases of Use of a 3- and 4-Variable Formulas to Differentiate Normal STE from Subtle LAD Occlusion