An 85-year-old female presents from her nursing home in the respiratory failure. EMS found the patient in agonal respirations. On arrival to the ED the patient is intubated, heart rate 150, blood pressure 40/palp, and she has palpable femoral pulses. As I run through possible next steps to keep this patient from impending arrest, EMS shows me the EKG. Should we activate the cath lab?
There are many conditions that can mimic ST segment elevation. Pericarditis, LBBB, paced rhythm, takotsubo’s stress cardiomyopathy, benign early repolarization, among others. Read a great review of these conditions here.
An uncommon “mimic” can be massive or sub- massive pulmonary embolism. The large clot burden causes right ventricular strain and transmural ischemia, and can show STEMI on ECG. The most commonly reported ECG “STEMI mimics” in massive PE are elevations in the anterior/lateral leads and inferior ST depressions and t-wave inversions. However, inferior ST elevations are also possible. In this nursing home patient who may be immobile, PE was at the front of my mind.
Tachycardia is another common reason to misdiagnose STEMI. With heart rates >130 it becomes more likely that ischemic ECG finding could be secondary to myocardial demand. Also consider atrial fibrillation and flutter because these can cause STEMI-like changes. Read here for more great pearls on ECG factors that lead to misdiagnosed STEMI.
For the case above, a medical student would be able to list off at least a dozen differential diagnoses for undifferentiated shock. STEMI seems as likely as others with inferior ST elevations on ECG. And I was feeling the added pressure of the door-to-balloon time clock ticking. Bedside ultrasound can be a useful tool to rapidly assess for other more likely causes. In massive PE, an apical 4-chamber view shows a dilated RV, and if you’re lucky you could find the culprit DVT.
STEMI may be one of the most time sensitive diagnoses to make in this case, but it’s important to take the extra moment to consider the possible mimics and always grab the ultrasound probe to evaluate for other causes when the clinical scenarios is not classic.
In the case we activated the catch lab, which did not show any RCA culprit lesion. A follow up CT PE was also negative. Despite diagnostic uncertainly the patient did well after aggressive resuscitation. If presented the case again I would certainly consider cath lab activation, but maybe first after discussion with the interventional cardiologist knowing the limitations of an ECG with HR>130 and atypical presentation.
- ST-segment elevation in V1-V4 in acute pulmonary embolism: a case presentation and review of literature. Omar HR. Eur Heart J Acute Cardiovasc Care. 2015. http://m.acc.sagepub.com.proxy.lib.ohio-state.edu/content/early/2015/09/15/2048872615604273.1.long?view=long&pmid=26373811
- Bedside Ultrasound to Evaluate Pulmonary Embolism Masquerading as ST Elevation Myocardial Infarction. Shy BD1, Gutierrez A1, Strayer RJ1.J Emerg Med. 2015 Jul 8. pii: S0736-4679(15)00483-7. doi: 10.1016/j.jemermed.2015.05.005. [Epub ahead of print] http://www.sciencedirect.com/science/article/pii/S0736467915004837?via%3Dihubm
- Zhong-Qun Z, et al. Correlation between ST-segment elevation and negative T waves in the precordial leads in acute pulmonary embolism: insights into serial electrocardiogram changes. Ann Noninvasive Electrocardiol. 2014 Jul;19(4):398-405. doi: 10.1111/anec.12115. Epub 2013 Nov 8.