M&M Discussion: MI presenting as GERD

M&M offers an opportunity to look at our clinical decisions and thought paradigms to address our frames and make the necessary changes to avoid harm to our patients. Check out the case below and the issues posed and let’s start some discussion. Answers to the questions are a combination of opinion and literature supported answers. Tell us what you think.

47 yo male history of GERD c/o chest pain for the past 4 days. The type of pain is typical of his GERD associated pain. Pt describes an acid taste in his mouth. Normal EKG, glucose 287. Omeprazole is administered and patient has marked improvement with but not complete improvement. Upon hearing that patient is still not completely better after waiting in ER for 8 hrs, the new attending coming on orders troponins and a repeat EKG. Troponins are positive and EKG shows new inferior wall and precordial changes.
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Issue: Should we be ordering troponin in patients who has chest pain but appears to have a clear cut non-cardiac diagnosis?

Can you say that this is not cardiac pain?. Article by Hollander (AEM 2007:14;210-15) found that in cases where doctor is sure patient has a non-cardiac problem (i.e. GI problem or musculoskeletal problem,) 4% of these patients will have an MI, death or revascularization within 30 days. This would support sending troponins in this patient with chest pain even though it is exactly like his previous episodes with “GERD”

Issue: Sending troponins on patients with low pretest probability, you are more likely to get False Positive than True Positive. However wouldn’t you rather have a False Positive than a False Negative?

The question is…do these patients who make troponins who are not having ischemia at risk for a worse prognosis? If it does help to know their troponins are elevated is it helpful to further monitor and follow them?

Issue: When blood sugar comes back at 287, should this change your view of patient since he now has a cardiac risk factor?

Yes.

Issue: Does response to H-2 blocker or Maalox change your mind about the diagnosis?

There is no literature that supports that response to H2 has any predictive value on the pain being cardiac or not.
Your decision depends on your pretest as a whole picture (i.e. if a crushing chest pain responds to H-2 blocker doesn’t mean anything but if low probability and sounds GI, response to H-2 may help confirm your view). Alternatively, no response or limited response to medication may make you expand your differential.

Issue: Should you make diagnosis of GERD in the Emergency Department?

Patient will be walking around with this diagnosis from the visit onward. What are the consequences when a diagnosis is made in the Emergency Department or in clinic.

Pearl: Do not tell the patient that he doesn’t have a cardiac problem. All you can say is that the patient’s symptoms are likely GI in origin and that a cardiac cause is very unlikely. You also have to let the patient know that there is chance we could be wrong and that if patient’s symptoms get worse or do not get better, return to the ER immediately

Issue: New onset bradycardia in a cardiac patient.

If patient is obese and has a heart rate of 62 and doesn’t have a history of bradycardia, you should consider whether the patient is having an inferior wall infarct to explain his bradycardia. if heart doesn’t go with the way patient looks (i.e. not an athlete), you have to take pause and consider ischemia. Literature does show that patients with heart rate >80 have an increased chance of sudden cardiac death and cardiovascular events and non-cardiac death. There is no literature, however, on predictive value of relative bradycardia
Pearls from Discussion:
– Know what you want from a consultant before calling them so you can direct them toward the right action if they start doing the wrong thing.
– Nitroglycerin is contraindicated in aortic stenosis as it is a preload reducer.
– Persistent chest pain with EKG changes can buy you ticket to cath lab even if no ST elevation.
– Dynamic EKG changes buy you a CCU bed

1 Comment on "M&M Discussion: MI presenting as GERD"

  • Should we send a troponin on patients with GI pain?

    In the only MI that I know I missed for sure, it was a 32 year-old with GI pain, 6 hour onset, and a normal ekg. All subsequent ekgs were normal despite knowing the patient had an MI. No one thought this guy had an MI.

    It is very low yield, so this depends on how you practice. If you want to pick up the 0.0001%, go for it. In this scenario, there are really no false positives. If you send a troponin on a patient with undifferentiated shock and it comes back +, then it might be a FP.

    Does the blood sugar of 287 make any difference?

    It is extremely ironic to hear the poster write “yes”, because all data says “no”, including Hollander’s. Risk factors are useless in patients over 40 years old. Look up articles like “Is this patient having an MI?”, and you’ll find the LR+ is about 1.0. The 47 year-old already has a risk factor, he’s 47 years old. Having an additional risk factor makes no difference whatsoever.

    The notion of diabetics having silent MIs is misleading. Anyone may have “silent” or unrecognized MIs. You might be having one now.

    If we can diagnose cad with maalox, we wouldn’t be wasting money on stress tests. More accurately, if we can diagnose cad with the equivalent of saline, we wouldn’t need stress tests. In RCTs, iv H2 blocker works as well as iv saline for tummy aches (they both make pain better). When I see a patient with maalox on his lips in the ED, that patient is marked for death.

    NTG is NOT contraindicated in a patient with AS, especially if it’s not critical. In a patient with critical AS, you have to be very careful with any BP agent. We can argue about the reason for this, but it’s not really because of a preload issue. Patients with bad AS cannot increase their stroke volume if you make them hypotense, so they may go to ground or go to sky if you lower their BP too much.

    What do you do with a patient with critical AS and STEMI? What do you do with a patient with critical AS, STEMI, and CHF?

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