It's an early Sunday morning and it hasn't gotten that busy yet. You decide to go to the cafeteria and get some breakfast. As you sit down to start shoveling in the Western Hash Browns, a patient pops up the board. It is a a male in his 30's with a chief complaint of "chest pain". You click your name on, but figure you have time to eat a few bites before going in the room when the patient care tech who wheeled him back comes and tells you "hey, that guy doesn't look so good".
When you walk in the room you are faced with a diaphoretic young, slightly overweight male who complains of 7/10 left-sided chest pain. It has been going on since yesterday and he states, "I thought it was my anxiety acting up but it didn't go away." He has a HR of 90 and a blood pressure of 115/80.
The tech wheels in the EKG machine and obtains the following EKG:
Looking at EKG #1 you are concerned about cardiac ischemia because of ST elevation in V3 associated with a hyperacute T wave and suggestion of ST depression in the inferior leads. After promptly telling your attending about the patient, ordering some labs and pain control you walk back in the room to check on him. The guy at this point looks decidedly peakish. You decide, as you should, to obtain a repeat EKG:
You have heard that a new LBBB can be an indication for cath lab activation, but a new RBBB? Since the effects of acute MI are related to ischemia, review of the blood supply to the conduction system is helpful when thinking about conduction defects in the setting of acute MI. While there is some variability from person to person, the basic breakdown is nicely illustrated by the following image from PCI pedia (http://www.pcipedia.org/wiki/Coronary_anatomy ):
As expected, disrupting the blood supply can lead to a number of conduction defects including complete heart block (usually RCA), RBBB (usually LAD) and LBBB (usually LAD). New bundle branch blocks occur in approximately 12% of all acute MIs (Ref 1).
Does development of a RBBB have prognostic value? Several papers from the Cardiology world have examined this for patients receiving either thrombolytic therapy or PCI. In general, developing a new RBBB is bad news. Patients with RBBB universally have higher overall 30-day mortality than those without conduction defects [33% vs 11.6% for those receiving thrombolytic therapy (Ref 2), and 14.0 % vs. 1.9 % for those receiving PCI (Ref 3)]. When examined, patients with new RBBB also had higher overall peak levels of CK-MB (expressed as x upper limit of normal) [16.6 (8.6 - 24.0) vs. 7.6 (3.1 - 14.9)]. These findings imply that patients who develop a new RBBB likely have a larger infarct size.
We are classically taught to activate the cath lab for patients with STEMI or new LBBB. Given the unreliability/lack of specificity of new LBBB for diagnosis of myocardial infarction, it has been removed as a hard criteria for cath lab activation in the latest iteration (2013) of AHA/ACCF guidelines (Ref 4). The current Universal Definition of acute Myocardial infarction is: "new ST elevation at the J point in at least 2 contiguous leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or of 1 mm (0.1mV) in other contiguous chest leads or the limb leads." According to the AHA, "New or presumably new LBBB has been considered a STEMI equivalent. Most cases of LBBB at time of presentation, however, are “not known to be old” because of prior electrocardiogram (ECG) is not available for comparison. New or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation."
But what about new RBBB? It is not currently part of AHA guidelines regarding cath lab activation for PCI, but should it be? New RBBB has an important differential diagnosis (including PE) which includes acute ischemia. A European study (Ref 5) that included patients from 8 different hospitals (mostly Czech as the Czech Society of Cardiology recommends primary PCI for any new BBB) addressed whether new RBBB in the absence of ST elevation should be considered as an indication for emergent PCI. Of a total of 427 patients with "acute MI and RBBB", 226 (53%) had associated ST-elevation. When these patients went to coronary angiography, 135 (67%) of patients with RBBB and no ST elevation has TIMI flow 0-2, compared with 205 (91%) of those with RBBB and ST-elevation. This is far from definitive evidence that we should be sending these all to the cath lab - but it suggests that we should, at the very least, factor new RBBB into our clinical decision making regarding chest pain management in the emergency department.
Coming back to our case...
After the call for cath lab activation but before the EKG leads are taken off the patient, he develops the following rhythm and then promptly stops talking:
You feel for a pulse and feel nothing. After several rounds of CPR and multiple shocks you get ROSC and the patient is taken to the cath lab where he is found to have a 100% occlusion of his LAD and is reperfused successfully:
|Cath lab report|
So what should you take home from this case?
1. Serial EKGs provide valuable information. In addition to evaluating them for new q waves, ST segment or T wave changes, close evaluation for new intraventricular conduction defects is mandatory in the assessment of potential cardiac ischemia.
2. If a patient with cardiac ischemia develops a new RBBB, be very afraid and prepare. These patients likely have proximal LAD lesions and large infarct sizes and are predisposed to sudden cardiac arrest (i.e. the "widow maker"lesion)
3. Young people can have heart attacks too. Saving lives takes vigilance.
Contributed by Maia Dorsett [@maiadorsett] PGY-3
Faculty Reviewed by Dr. Doug Char
Special thanks to Dr. Heather Webb [@webbmd)]at Barnes St. Peters for the great case (and the life saved).
1. Sørensen, J. T., Stengaard, C., Sørensen, C. A., Thygesen, K., Bøtker, H. E., Thuesen, L., & Terkelsen, C. J. (2013). Diagnosis and outcome in a prehospital cohort of patients with bundle branch block and suspected acute myocardial infarction. European Heart Journal: Acute Cardiovascular Care, 2(2), 176-181.
2. Wong, C. K., Stewart, R. A., Gao, W., French, J. K., Raffel, C., & White, H. D. (2006). Prognostic differences between different types of bundle branch block during the early phase of acute myocardial infarction: insights from the Hirulog and Early Reperfusion or Occlusion (HERO)-2 trial. European heart journal, 27(1), 21-28.
3. Kurisu, S., Inoue, I., Kawagoe, T., Ishihara, M., Shimatani, Y., Hata, T., ... & Kagawa, E. (2007). Right bundle-branch block in anterior acute myocardial infarction in the coronary intervention era: acute angiographic findings and prognosis. International journal of cardiology, 116(1), 57-61.
4. de Lemos, J. A., & Ettinger, S. M. (2013). 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. Journal of the American College of Cardiology, 61(4).
5. Widimsky, P., Roháč, F., Štásek, J., Kala, P., Rokyta, R., Kuzmanov, B., ... & Lorencová, A. (2012). Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy?. European heart journal, 33(1), 86-95.
Interested in learning/reviewing some more? Here are some related FOAMed resources:
Young people with Acute MI? Happens, sure does. Click here for an interesting case by Amal Mattu.
Early EKG changes in acute MI? Watch out for hyperacute T waves. Learn more about them from Steve Smith's ECG blog entry on the topic here.
What if the patient has a pre-existing LBBB? You can still diagnose STEMI. See more with Steve Smith's explanation and paper on Modified Sgarbossa criteria.
When its wide and fast sometimes it hard to tell if its Vtach or SVT with aberrancy: learn how to tell the difference from the group at Life in the Fast Lane here.