A 70 something with history of coronary disease and pulmonary embolism presented with sudden onsent chest pain, diaphoresis, and abdominal pain 2 hours prior. BP was 70s/30s. acute shock (cold and clammy and hypotensive and abdominal pain).
The first thing to do in shock is look at cardiac function:
Obviously the left ventricular function is very poor, and there is a dense wall motion abnormality. So this is consistent with acute Occlusion MI. The RV was not enlarged.
Acute cardiogenic shock with chest pain is either large acute Occlusion MI, acute Valve rupture, acute myocardial rupture, acute hemopericardium, or acute Pulmonary embolism. The bedside echo tells you that LV function is terrible, the RV is actually small, there is no pericardial fluid. So this is acute MI until proven otherwise, even without the ECG.
Next we need to record an ECG:
What do you think?
This shows a ventricular paced rhythm with multiple leads confirming occlusion MI (OMI) by the Smith Modified Sgarbossa Criteria: There is proportionally excessively discordant ST Elevation in all inferior leads (lead III has 3.5mm divided by 5 mm = 70%. Just one lead with a ratio > 25% is highly specific for OMI in ventricular paced rhythm. Leads V5-6 also have a ratio > 25%. There is proportionally excessively reciprocal discordant ST depression in aVL (>30% in 1 lead is 100% specific!). There is concordant ST depression in V2 (again, this ALONE is enough to make the diagnosis).
See this paper we wrote (senior author is Smith): Dodd KW, Zvosec DL, Hart MA, et al. Electrocardiographic Diagnosis of Acute Coronary Occlusion Myocardial Infarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria. Ann Emerg Med [Internet] 2021;Available from: http://dx.doi.org/10.1016/j.annemergmed.2021.03.036
If you don’t see it, perhaps looking at a recent previous ECG will help:
Let’s put them one ontop of each other so you can see them both at once; here again is the presentation ECG in shock:
Is there any doubt about what is going on?
Unfortunately, the Queen is not certain. But “indeterminate” by the Queen of Hearts is still very specific, and combined with an extremely high preteset probability it is clearly Acute OMI causing cardiogenic shock.
Unfortunately, the providers were not convinced of MI. The cardiologists thought he was “too unstable” to go to the cath lab.
They took the patient for a CT scan because of worry for PE, and due to abdominal pain. They gave pressors. They thought about LV assist devices, ECMO, etc.
Here is the portion of the CT which shows the heart:
Notice areas of extreme blotchy hypoperfusion of the myocardium. This is due to acute coronary occlusion. Again, the RV is much smaller than the LV.
The patient also had a time-consuming formal echo before going to cath:
EF = 20%. Regional wall motion abnormality-akinesis of apical, lateral, mid-to-basal anterolateral, apical inferior, mid-to-basal anterior, mid-to-basal inferolateral.
All consistent with acute coronary occlusion.
In my view, this is obvious acute cardiogenic shock due to acute coronary occlusion. There should have been no delay to the cath lab. “Too unstable” is in my view not a reason.
I would say to my interventionalist: “the only way the patient will survive is with IMMEDIATE revascularization. If he dies on the way to the cath lab or in the cath lab, so be it. There is no such thing as “too unstable” to get the only therapy which can save the patient.”
There was almost 5 hours between arrival and angiogram:
Culprit Lesion (s): Suspected culprits include acute occlusion of the ostial ramus and culprit stenoses of the proximal and mid circumflex.
The patient died.
Learning Points:
- Learn to diagnose OMI in the setting of Ventricular Paced Rhythm. It is not that hard!!
- In Cardiogenic shock from OMI, Coronary intervention is what will save the patient!
- Never delay intervention because the “patient is too unstable.”
- If you did not have PCI capability, thrombolytics would be indicated!
- Mortality in cardiogenic shock is high, but with prompt revascularization, mortality can be greatly reduced. see 2 studies below.
Mean time to revascularization was 12 hours in this study, and mortality was 50% in both groups (“early” revasc vs medical therapy) Hochman JS. EARLY REVASCULARIZATION IN ACUTE MYOCARDIAL INFARCTION
COMPLICATED BY CARDIOGENIC SHOCK. New England Journal 1999.
Saito Y et al. Door-to-Balloon Time and Mortality in STEMI With Cardiogenic Shock: A Nationwide Registry. JACC Asia 2024;4(5):421-2
This article by Saito shows that a short door to balloon time in Cardiogenic shock had mortality of 17%, which is far better than in the above study due to fast intervention!!
Results:
In-hospital mortality was higher in patients with Carddiogenic shock (CS) and cardiac arrest (CA), followed by those with CS and no CA and those without CS (36.7% vs 17.0% vs 2.3%; P < 0.001). Notably, door-to-balloon time had a positive correlation with observed and adjusted in-hospital mortality in patients with STEMI and CS (Figure 1). Multivariable analysis identified shorter door-to-balloon time as a factor associated with better survival (OR: 1.07; 95% CI: 1.05-1.09; P < 0.001). The door-to-balloon time was significantly associated with in-hospital mortality in the subgroups of CA, MCS device use, and hospital volume, and the effect of shorter door-to-balloon time on survival was more pronounced in patients without CA or MCS device use, although the differences in relative mortality between the presence and absence of CA or MCS device use were small.
We don’t know if the patient could have been saved. No one will ever know. But every minute of delay is myocardium lost. From the time of onset of chest pain to 4 hours — 80% of the mortality benefit of thrombolytics is lost. From hour 2 to hour 4, 60% is lost. In this case, the delay was 7 hours from onset of chest pain.
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MY Comment, by KEN GRAUER, MD (3/2/2026):
In the past — Pacemaker tracings were more problematic because of the dictum that used to be routinely cited ==> “You cannot diagnose an acute MI when the patient has a pacemaker”. This dictum has long since been proven false in many (if not most) cases of pacemaker patients who present with new-onset CP (Chest Pain).
- An especially illustrative example of how a completely paced ECG may be diagnostic of acute OMI was highlighted in the August 20, 2019 post (See My Comment at the bottom of the page in this 8/20/2019 post — as well in other examples from Dr. Smith’s ECG Blog in which Smith-Sgarbossa criteria diagnostic for acute MI are satisfied despite an ECG that is completely paced).
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The Initial ECG in Today’s CASE …
As per Dr. Smith’s above discussion — Despite the fact that the initial ECG in today’s case is completely paced, it is diagnostic of an extensive ongoing acute STEMI.
- Especially given that the 70-something year old man in today’s case presented with new CP and in shock (BP = 70/30 mm Hg — with cold, clammy extremities) — the tracing that I’ve reproduced and labeled in Figure-1 needs to be recognized as the acute STEMI that it is.
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Review of the ECG Findings in Figure-1:
As per Dr. Smith — the diagnosis of an acute ongoing event becomes obvious as soon as the previous ECG on today’s patient was found (bottom tracing in Figure-1). But the diagnosis of an acute STEMI should be obvious even without access to the previous tracing.
- I favor the concept of proportionality as the most helpful clue for determining if ST-T wave changes that shouldn’t be there are (or are not) present.
- In Figure-1 — My “eye” was immediately drawn to the coved (“frowny” configuration) ST elevation in lead III (within the RED rectangle in ECG #1). Given modest depth of the S wave in lead III — the amount of J-point ST elevation is clearly disproportionate. Confirmation that this ST elevation is an acute finding in this hypotensive 70s man with new CP — is forthcoming from: i) Similar disproportionate ST elevation in the other 2 inferior leads (= leads II and aVF); — and, ii) The finding of equally disproportionate reciprocal ST depression in lead aVL.
Regarding the Chest Leads in ECG #1:
- In isolation — it might be difficult to determine if the peaked T wave in lead V2 of ECG #1 is or is not hyperacute. That said — it’s far more effective to begin with assessment in leads for which we know that ST-T wave appearance is not “normal”.
- The nearly equal amplitude of the overly “bulky” T wave in lead V4, compared to the S wave in this lead — is clearly abnormal in this hypotensive patient with new CP (within the BLUE rectangle).
- Similarly — neighboring leads V5, and then V6 — manifest no more than tiny paced QRS complexes, which are associated with disproportionately “bulky” T waves large enough to “swallow” these tiny paced QRS complexes within them.
- In the other precordial lead direction — the T wave in neighboring lead V3 also looks disproportionately enlarged compared to the modest S wave in this lead.
- And, now seen in context — I suspect the prominent T wave peaking that we see in lead V2 is likely to also represent hyperacuity.
- Putting It All Together: No less than 9/12 leads in ECG #1 are abnormal. Taken together in this hypotensive patient with new CP — this ECG is diagnostic of an acute anterior STEMI until proven otherwise.
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Figure-1: Comparison between the 2 ECGs shown in today’s case. Note the marked change in ST-T wave appearance in today’s initial ECG —compared to the previous ECG on this patient.
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