A previously healthy, well-appearing 42-year-old female living in a modern, high-rise apartment in downtown Los Angeles calls 9-1-1 at 5:30 am complaining of worsening of a burning, epigastric pain she had been experiencing for the last three days. She reports associated nausea and non-bloody, non-bilious vomiting, and that she couldn’t manage to get comfortable in bed until she finally decided to call for help at daybreak.

During her 9-1-1 call, she reports “pain, like heartburn, that just woke me up again and I had to throw up, … and then I was sweating so much.” Using the Los Angeles Tiered Dispatch System, the 9-1-1-telecommunicator couldn’t discern whether the patient was actually having abdominal or chest pain and opted to dispatch a chest pain (age > 40) dispatch code, launching a paramedic unit from the busy downtown fire station.

Upon arrival, paramedics find a young, fit-appearing Hispanic female sitting in her living room, reporting a “burning sensation in her throat.” She tells medics that she has a history of acid reflux but states that she wasn’t having any relief with her usual Tums. She also states that she usually feels like this after drinking alcohol, and that she had a few drinks last night and smoked some marijuana.

Her vital signs are within normal limits, her abdominal exam was benign, and she requests “something to help with her reflux,” but she ultimately refuses transport to the ED.

No further testing is performed, and her final paramedic provider impression was “non-traumatic abdominal pain/swelling”.

Three hours later, she walks into her primary care doctor’s clinic, where her internist notes her to be anxious, hypertensive and unable to tolerate liquids by mouth. He refers her to the University Hospital’s Urgent Care Center to “get some fluids before she goes home to rest.”

In the urgent care clinic, the patient gives a more complete history of three days of burning, aching epigastric pain radiating to the back. The pain was unrelated to exertion, however, the patient admits that she had recently worked out in the gym more than usual. She reports a past medical history of psoriatic arthritis for which she was taking infliximab (Remicade). She has no known history of cardiac risk factors (i.e., hypertension, diabetes, hyperlipidemia, obesity, family history of coronary artery disease, or tobacco use. Her blood pressure is hypertensive to 200/81 mmHg, she’s slightly diaphoretic but in no respiratory distress and with a benign abdominal exam.

IV access is established, and the patient is given 1 L normal saline and 4 mg ondansetron. A 12-lead electrocardiogram (ECG) was ordered, which showed no ST elevations, but mild diffuse depressions in II, III, and aVF as well as V4–6. (See Figure 1.) There is also subtle elevation and flattening of the ST-segment in lead aVR. The patient is given a “GI cocktail” of Maalox, viscous lidocaine and donnatal, with no relief. However, her pain does calm down after a dose of sublingual nitroglycerin.

A serum troponin (normal range < 0.01 ng/mL) was ordered and was found to be 35.0 ng/mL.  The patient receives 162 mg aspirin and nitroglycerin paste that decreases her systolic blood pressure to 154 mmHg. The patient is started on an unfractionated heparin drip and cardiology is consulted.

Shortly after, the patient is taken to the cardiac catheterization lab where she’s found to have multivessel coronary artery disease, including a 100% occlusion of her left circumflex artery, a 90% stenosis of her distal right coronary artery and 60% stenosis of her mid left anterior descending artery along with akinesis of the lateral left ventricular wall.

Four days later, she successfully undergoes a three-vessel coronary artery bypass graft (CABG), is subsequently found to have a stable ejection fraction, and is discharged home on oral medications for her heart (and reflux).

Figure 2 (a–d): Cardiac angiography consistent with multivessel coronary artery disease
2a: Schematic view of angiographic findings
2b: Left circumflex artery occlusion
2c: Left anterior descending artery with mid-vessel stenosis
2d: Right coronary artery with significant mid- and distal-vessel stenosis


Heart disease is the leading cause of death in the United States.1 This year, 720,000 Americans will have a new coronary event—defined as first hospitalized myocardial infarction (MI) or coronary heart disease death—and around 335,000 will have a recurrent event. Approximately 35% of people who experience a coronary event in a given year and around 14% of patients who have an acute coronary syndrome will die from it.1 Roughly 60% of patients with an acute coronary syndrome are transported to the emergency department via ambulance.2–4.

Up to one-third of patients experiencing an MI may not complain of chest pain, but rather present with atypical symptoms such as nausea, weakness and shortness of breath.5 Women, the elderly, and patients with diabetes are at higher risk of presenting with atypical symptoms.2,3,6 Patients who present with atypical symptoms are less likely to have prehospital ECGs performed and are more likely to have longer elapsed times from first prehospital medical contact to percutaneous intervention.2,7

In 2015, the Los Angeles Fire Department had over 391,000 unique EMS incidents, including 31,499 dispatches categorized as chest pain; 14,101 incidents with a prehospital provider impression of chest pain; and 2,607 ST-elevation myocardial infarctions (STEMIs).

On review of records from 2010–2015, 90% of cath-lab confirmed STEMIs among males were dispatched as chest pain, whereas 80% of such cases among females were dispatched as chest pain—meaning in 1 in 5 cases the dispatch may point the responding units in a different direction due to atypical symptoms described during the 9-1-1call.8

In this case, the 9-1-1 telecommunicator categorized the dispatch as chest pain. Responding paramedics did a thorough assessment of the client’s abdominal pain. However, they appeared to have anchored in on the “common and not life-threatening” etiology of the patient’s symptoms—suggestive of gastroesophageal reflux disease (GERD) or perhaps acute gastroenteritis.

Red flags in this case included the patient’s lack of response to medication that typically improve her symptoms, inability to tolerate food/liquid by mouth, diaphoresis, lack of abdominal tenderness, and being awakened from sleep due to her pain. The presence of associated diaphoresis on clinical exam also warrants attention, as this finding alone was found on one review to have the same likelihood ratio for the presence of acute coronary syndrome as exertional symptoms in emergency patients with chest pain.9

The ability to acquire 12-lead ECGs has been transformative in prehospital care, permitting screening of on-scene patients with chest pain for arrhythmia, ischemia and STEMI. Prehospital activation of the cath lab has resulted in decreased times from first medical contact to percutaneous intervention,10 and even improved survival in one study.11,12 It’s unclear if these benefits are equally distributed among both males and females using 9-1-1 to access cardiac care and how often ECG is used among groups at risk for atypical presentations.

Although this patient refused transport, a screening ECG in light of her other symptoms would have been ideal. Had an ECG been performed, there’s also the possibility that her diffuse subtle depressions without reciprocal changes wouldn’t have been recognized as critical disease. However, a patient with an ECG showing ischemic changes mandate LAFD paramedics to make a patient refusal of transport into a formal against medical advice (AMA) with base station contact and electronic transmission of the ECG. Had this patient not had access to timely primary care and incidental evaluation by an emergency physician, this patient contact in the field very well may have been her last.

This patient, though fit and reporting recent exercise workouts without exertional chest pain, did have a comorbidity and medication that weren’t noted on prehospital evaluation. Psoriatic arthritis in and of itself isn’t associated with increased risk of acute coronary syndrome, however infliximab—a biological cytokine inhibitor increasingly used in inflammatory bowel disease and various arthritidies—has been associated with increased incidence of acute MI.13

Emergency providers of all levels of training have the unique challenge and opportunity to seek out worst-first pathology in all patient presentations—especially among patients activating 9-1-1 who have already stratified themselves into a unique group. All of us have attended young or middle-aged patients with burning epigastric pain and immediately considered benign diagnoses that are treated with supportive care.

Lessons Learned

1. Patient context:  It’s important to ask why this specific patient (otherwise in good health, housed, and with good access to care) is calling at 5 am for an emergency, and recognizing this as a red flag.

2. Careful review of the dispatch code: Field personnel are usually not privy to the dispatch audio in real time, however, key hints at underlying concerning pathology are often expressed and may be indicated based on the dispatch code selected. Speaking to the person who called 9-1-1, reviewing the rationale for why a given dispatch code was selected, and evaluating the patient through history, physical exam and point of care testing based on this dispatch code is imperative.

3. Awareness of patients at high risk for atypical presentations: Sometimes simply saying out loud that a patient fits the profile of someone who is more likely to present atypically, including patients who are female, elderly, diabetic, on unique medications or who have limited English proficiency.

4. Deliberate review of tests to look for worst-first presentation: Some of the best cardiologists can tell a patient story based on an ECG, and we should all strive to at least reconcile patient symptoms with potential ECG findings.

5. Potential mimics: Inferior cardiac ischemia may present as epigastric abdominal discomfort, mimicking benign GI conditions such as reflux, peptic ulcer disease, esophagitis, or gastritis.

6. Thorough history and review of medications: Patients, including younger patients, are increasingly on medications with complex mechanisms of action and potentially severe adverse side effects. If it’s a medication you haven’t heard of, consider it has life-threatening side effects you haven’t heard of until proven otherwise or you are able to look up its side effects via an online medication resource.


1. Benjamin EJ, Virani SS, Callaway CW, et al. Heart disease and stroke statistics—2018  update: A report from the American Heart Association. Circulation. 2018;137(12):e67–e492.

2. Diercks DB, Kontos MC, Chen AY. Utilization and impact of pre-hospital electrocardiograms for patients with acute ST-segment elevation myocardial infarction: Data from the NCDR (National Cardiovascular Data Registry) ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry. J Am Coll Cardiol. 2009;53(2):161–166.

3. Coventry LL, Finn J, Bremner AP. Sex differences in symptom presentation in acute myocardial infarction: A systematic review and meta-analysis. Heart Lung. 2011;40(6):477–491.

4. Coventry LL, Bremner AP, Jacobs IG, et al. Myocardial infarction: Sex differences in symptoms reported to emergency dispatch. Prehosp Emerg Care. 2013;17(2):193–202.

5. Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA. 2000;283(24):3223–3229.

6. Canto JG, Goldberg RJ, Hand MM, et al. Symptom presentation of women with acute coronary syndromes: Myth vs reality. Arch Intern Med. 2007;167(22):2405–2413.

7. Cannon AR, Lin L, Lytle B, et al. Use of prehospital 12-lead electrocardiography and treatment times among ST-elevation myocardial infarction patients with atypical symptoms. Acad Emerg Med. 2014;21(8):892–898.

8. Baciak K, Sanko S, Eckstein M. Gender disparities in the prehospital setting among known ST-segment elevation myocardial infarction patients. Prehosp Emerg Care. 2018;22(1):101–150.

9. Fanaroff AC, Rymer JA, Goldstein SA, et al. Does this patient with chest pain have acute coronary syndrome?: The rational clinical examination systematic review. JAMA. 2015;314(18):1955–1965.

10. Squire BT, Tamayo-Sarver JH, Rashi P, et al. Effect of prehospital cardiac catheterization lab activation on door-to-balloon time, mortality, and false-positive activation. Prehosp Emerg Care. 2014;18(1):1–8.

11. Studnek JR, Infinger A, Wilson H, et al. Decreased time from 9-1-1 call to pci among patients experiencing stemi results in a decreased one year mortality. Prehosp Emerg Care. 2018;22(6):669–675.

12. Koul S, Andell P, Martinsson A, et al. Delay from first medical contact to primary PCI and all-cause mortality: A nationwide study of patients with ST-elevation myocardial infarction. J Am Heart Assoc. 2014;3(2):e000486.

13. Low AS, Symmons DP, Lunt M, et al., Relationship between exposure to tumour necrosis factor inhibitor therapy and incidence and severity of myocardial infarction in patients with rheumatoid arthritis. Ann Rheum Dis. 2017;76(4):654–660.