This case is posted by Salim Rezaie (@srrezaie)
Chest Pain, “Negative” Stress Tests, POCUS, & ECG Equations
It has some peer review by me at the end, so we're co-posting!!
Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations
by Salim Rezaie
Chest Pain, “Negative” Stress Tests, POCUS, & ECG Equations
It has some peer review by me at the end, so we're co-posting!!
Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations
by Salim Rezaie
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 less than 24 hours.
I asked Dr. Smith to give some expert peer review as well:
I asked Dr. Smith to give 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 [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 [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 [3]
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 ultrasounding 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)
The Evidence [4]: 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
Stephen W. Smith, MD
Hennepin County Medical Center (HCMC Minneapolis, MN Twitter:@smithECGBlog Blog:Dr. Smith’s ECG Blog |
Salim,
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 theT/QRS ratio is
greater than 0.36, then acute STEMIis 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.
References:
- 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
After following this blog for a few years, the first ecg jumped out to me as obvious LAD territory ischemia. Q + hyperacute T clinches the diagnosis, in a patient with considerable a priori odds. There is also some inferior ST depression, reciprocal to injury to the high lateral wall (occlusion proximal to OM1?).
ReplyDeleteBest regards,
Maarten Van Hemelen
IM resident
comment 1: Yes!
Deletecomment 2: Proximal, yes, but proximal to D1 (OM1 is off the circ)