STEMI MIMICS:
There are several STEMI imposters out there, and memorizing them all can be difficult, so I am going to cover the most commonly encountered ones.
Left Bundle Branch Block:
In order for a QRS complex to be narrow (0.08-0.12 seconds), the impulse from the SA node must travel through the AV node and down both the left and right bundle branches at the same time. In a LBBB the left bundle does not conduct the impulse. This means that the electrical signal must travel down the right bundle branch and then travel across the heart to the left ventricle. This takes longer and results in a wide QRS. The LBBB also presents with elevation of the ST-Segment, although it is not due to myocardial ischemia, sometimes. I say sometimes because a LBBB can hide true ST-Elevation, and an MI with a new LBBB has a very poor prognosis. For this reason, we have to be careful in the setting of chest pain. There are, fortunately some things that help us out. First, the one thing that differentiates a LBBB from a STEMI is dynamic changes. A LBBB should not evolve during subsequent 12-leads. If you notice further elevation from the baseline ECG, reciprocal changes, or other abnormalities such as T-wave inversion, you need to consider this a potential STEMI. Second we have the Scarbossa Criteria for LBBB. This was developed by Dr.Scarbossa to solve this problem, and it was further modified by Dr.Smith to include a higher percentage of patients what were being missed with the original criteria. In order to call STEMI on a LBBB, look for the following criteria:
Concordant ST elevation in leads with a positive QRS, in at least 2 leads, where elevation is >1mm.
Concordant ST Depression in any 2 leads V1-V3 where elevation is >1mm.
Discordant ST elevation in any 2 leads with a negative QRS where the height of the J-point is at least 25% the depth of the preceding S wave.
If the patient meets any of the above criteria, this is a STEMI Equivalent, and the cardiologist needs to be contacted regarding activation of the cardiac cath lab.
Hyperkalemia:
Hyperkalemia occurs when the serum (extracellular) level of potassium in the blood reaches a level >5.0mmol/L. When this happens we see characteristic changes, including widening of the QRS globally on the 12-lead, and tall “peaked” T-waves. As levels climb higher, we have flattening of the P-wave, and eventually the forming of a Sin wave as the QRS and T waves both widen. This eventually will progress to ventricular tachycardia, then ventricular fibrillation, and finally asystole. Make no mistake, this is a serious medical problem, BUT, it is not a STEMI. What typically leads to misreading of the ECG is mistaking the peaked T-waves for ST elevation. The other problem is that these patients often present similarly to those with myocardial ischemia. Hyperkalemia causes nausea, weakness, and ascending muscle paralysis, as well as cardiac dysrhythmias. The populations most prone to it are those with significant renal dysfunction, dialysis patients, and diabetics. Some patients with profound hypomagnesemia may also present similarly. We can still use serial ECGs to look for dynamic changes, and other abnormalities to try and rule out STEMI. Peaked T-waves can be a precursor to STEMI, but they usually occur right before elevation, meaning a repeat ECG will probably catch the change early. Use caution with these patients, because, if it is hyperkalemia, we want to identify that fact and treat following that protocol rather than treat for ischemia.
Left Ventricular Hypertrophy (LVH):
LVH can occur for a number of reasons, ranging from hypertrophic cardiomyopathy to genetic factors. In LVH the myocardial tissue of the left ventricle is enlarged and presents a higher amplitude QRS complex when depolarization occurs. There are a few different ways of identifying it, but the rule of 35 is probably the easiest. Take the depth of the largest S-wave in V1 or V2 and add it to the height of the largest R-wave in V5 or V6. If they add up to more than 35mm, LVH is confirmed. LVH mimics a STEMI in that it too will produce some degree of ST elevation that is not related to myocardial ischemia. Again, we can rely on dynamic changes here because LVH does not change between 12-leads. If the elevation increases, its probably a STEMI.
Brugada Syndrome:
Although not a STEMI, Brugada is an equally troubling finding. Brugada syndrome is a Sodium channel abnormality that leads to the development of paroxysmal V-tach or V-fib. It often kills patients a a young age, and without any warning. If it is noted on an ECG, we need to transport the patient; although cath lab activation is not warranted here. The most common ECG presentation of Brugada, and the one that most-mimics a STEMI is a Type 1 presentation. These patients will have “coved” ST-segment elevation in any lead V1-V3, immediately followed by a negative T-wave. If confirmed, the patient will likely need in implanted ICD to prevent sudden death at some point in time.
Pericarditis:
This is less common than some of the other mimics, but it may be the most easy to mistake for STEMI. In pericarditis, there is inflammation of the pericardial sac around the heart. This presents with a burning chest pain, that is exacerbated by lying supine, and palliated by leaning forward. While gestalt alone is not sufficient to diagnose this disorder, it does provide a good indication for us to look closer at the 12-lead. Patients with pericarditis will present with diffuse/global ST-elevation in all, or the majority of, the leads on a 12-lead. The elevation also often has a characteristic J shaped upslope that resembles half of a “happy face”. If pericarditis is suspected, a call to the cardiologist is warranted prior to activation of the cath lab.
These mimics are not the only ones, and it is worth taking the time to get a second opinion on any questionable 12-lead. I have only presented the ones that are very commonly mistaken for STEMI, and a future Ebook will cover more territory here. Remember, if in doubt, activate the cath lab. It is better to overtreat a patient and get yelled at by an angry cardiologist than it is to sit in front of a jury.
Comments