Back when I was working as a paramedic I would love to write papers on detailed topics. STEMI's were one of those topics that brings a different feeling to everyone when thought of. Initially when learning about them in school it seemed easy, "Oh those squigglies are big looking! Here is your medicine sir!". However, you swiftly realize that there are so many variables to heart tissue death. It's not as easy as just walking in and relaying the books knowledge to a dynamic body system. People are so different from one another, and family history is never written in the open. That skinny guy that looks healthy may have some of the worst arteries you'll ever see. Because of this I always recommend to stay vigilent and remain humble. The day you let your guard down is the day that foot cramp (with no other discernible signs/symptoms) will bite you in the ass.
Below is a paper that I wrote for fun if you believe that. I enjoyed writing on topics that helped myself learn, and when I had Paramedic students under me it served as a good resource.
Oringally written on Wednesday, May 8, 2019
06:00
12-Lead EKG's are an important part of a paramedic's arsenal of tools. However, is it always reliable? In just one ED study, they found that ST-elevation only accounted for 15-31% of Acute Myocardial Infarction(AMI). Of course we must take with a grain of salt that this was just a single study done out of one ED, but as we all have seen in the field; this study does represent a lot of cases. Since the inception of our license and time in the field, we have begun to build our course of actions. We have seen numerous calls, but one of the most prevalent calls we receive is chest pain. Most of the chest pain calls that have been received lately in my ambulance have been related to respiratory or musculoskeletal. With that being said we cannot neglect our cardiac patients. These patients usually have multiple co-morbidities, and the cause of cardiac was from many years of other illnesses putting strain on the overall system. That is a topic for another rant! Today, as you may have noticed with my transition here, will be cardiac related. More specifically it will be regarding the topic of STEMI imposters. At some point I'll discuss some STEMI imposters, and ways they will stand out.
I began with this topic because of one of our medic students. He had a recent ride along with our CES coordinator (clinical education specialist), and our student was a little worried. Our CES hit him with his first "pimping". You see, medic students would always get "pimped". This wasn't really anything negative. Doctors, senior medics, and senior nurses are very knowledgeable and they love spreading that knowledge. Our field requires such a vast amount of knowledge that knowing every little detail is difficult to do. Some of us don't know where to look, and need a little nudge. So what our CES did was improve the general knowledge of our student by making him reach out to learn it. Rather than telling the answer. So I spoke with him a little on it, and was inspired to also write about it.
STEMI imposters is a fun topic, because it builds on a fundamental skill of recognizing ST elevation. ST elevation is a key component in recognizing where an acute myocardial infarction (AMI) could be originating, and as a new medic that know how is needed. As you progress as a student though, you realize that there are multiple other conditions or illnesses that could represent ST elevation. Recognizing these is a big part of diagnostic measures that may ultimately lead to treatment measures. Do you want to be a minimalist medic that may use phrases like, "it's in my protocols, so I just did it"? That is a lazy excuse to treat patients. Especially since a human body is dynamic, and no two calls are the same. Embrace knowledge as a sentiment to help any and every patient you may come across in the best manner possible.
So before we talk a little about our ST elevations mimicry, we should all agree that having an imposter rhythm does not rule out an actual STEMI. If you have a strong index of suspicion that your patient is having a AMI then treat as such. There is a way to help identify AMI through certain imposter rhythms, but not all. While on that topic we will begin with that method: Sgarbossa's Criteria. This method was developed by Dr. Elena Sgarbossa in 1996. Simply put Sgarbossa's relies on "inappropriate concordance or excessive discordance".
Her criteria will help you see past two imposter rhythms. Which are your LBBB and paced ventricular rhythms. Before her criteria was accepted, these rhythms were deemed to be imposters but you'd still treat symptoms. Now her criteria will deliver great accuracy. In a typical LBBB we would usually see the j point moved in an opposite direction of the complex, even being above/below the isometric line. This is known as "discordance", and it is normal to see in your LBBB and paced rhythms. Now if you were to see greater than 5mm of "discordance" in your rhythms then you should increase your index of suspicion, however doesn't prove AMI unless you have "concordance" of 1mm or greater. With concordance you can almost guarantee AMI.
AHA! Now for the Imposters that you have all been waiting for. Beginning with left bundle branch block (LBBB), because of it's appearance last paragraph. LBBB occurs when there is a problem with the left branch of the electrical conduction system. So the electrical pathway must travel elsewhere to complete it's beat. This causes the beat to back track and then travel down the right branch instead. Once the impulse reaches the right ventricle via the right bundle branch, it then travels to the left ventricle via the septum. This also makes the left ventricle contract a little later than it would for a normal beating heart. This may also cause the heart to eject blood less efficiently out of the left ventricle. This rhythm is easily managed, unless you have underlying heart failure. This may or may not always be an ongoing beat, in some cases exercise may bring on the arrhythmia. These heart conditions may cause a LBBB, but are not limited to: CAD, HTN, cardiomyopathy, myocarditis, MI, congenital heart diseases, certain medicines, aortic stenosis, hyperkalemia, digoxin toxicity. LBBB may exacerbate SOB, due to worsening ejection at left ventricle especially in heart failure. More specifically, the LBBB has:
• Extended QRS to >120ms, and eliminates the normal septal Q waves in the lateral leads (I, v5-6).
• The overall direction of depolarization (from right to left) produces tall R waves in the lateral leads (I, v5-6), and deep S (V) waves in the right precordial leads (V1-3), and usually leads to left axis deviation.
• As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (M shaped) R waves in the lateral leads.
ECG diagnostic criteria includes:
• QRS >120ms
• Dominant S wave in V1
• Broad monophasic R wave in lateral leads (I, aVL, V5-6)
• Absense of Q waves in lateral leads (aVL may have small q waves)
• Prolonged R wave peak time >60ms in left precordial leads (V5-6)
ECG QRS Morphology:
QRS in Lateral Leads
-R Wave in lateral leads may be:
• 'M' shaped
• Notched
• Monophasic
• RS complex
-QRS in V1
• rS complex (small R wave, deep S wave)
• QS complex (deep Q/S wave with no preceding R wave)
Some things to also note regarding LBBB:
• It is unusual for LBBB to exist in the absence of organic disease. New LBBB in the context of chest pain is traditionally considered part of the criteria for thrombolysis. However, new onset LBBB have little increased risk of acute myocardial infarction at the time of presentation.
• Differential diagnosis is Left ventricular hypertrophy (LVH) and may produce a similar appearance to LBBB, with QRS widening and ST depression/T-wave inversion in the laterals.
• An incomplete LBBB is diagnosed when the typical LBBB morphology is associated with a QRS duration <120ms (less than).
Next up on our list of STEMI imposters we have Benign Early Repolarization (BER). BER is most commonly seen in our younger patients of <50 years of age. A typical patient seen may be a young, somewhat athletic individual that is otherwise healthy. BER has usually been seen in typically healthy individuals, however, some studies have shown a correlation in some dysrhythmias, ventricular fibrillation and death. Be sure not to diagnose over the age of 50, and especially not over 70. These age groups are more likely presenting actual myocardial ischemia. BER may mimic pericarditis, or MI. BER is also something that may be intermittent and not always occurring, just like our LBBB.
ECG Characteristics include:
• J-point elevated 1mm or more in two or more adjacent leads, often with a notching or slurring in the inferior leads (II, III, aVF).
• Generalized concave ST elevation in the precordial (v2-v6) and limb leads (I,II, III, aVF).
• Prominent, slightly asymmetrical T waves that are concordant with the main vector of the QRS complexes.
• The degree of ST elvation is modest in comparison to the T-wave amplitude (less than 25% of the T wave height in V6).
ST segment/T wave morphology:
• There is elevation of the J point
• T wave is peaked and slightly Asymmetrical
• ST segment and the Ascending limb of the T wave form an Upward concavity.
• Descending limb of the T wave is straighter and slightly steeper than the ascending limb.
J-point morphology is a characteristic feature of BER. One will notice a "notched" or irregular J-point. This is also called a "fish hook" pattern. It's definitely one of those "once you see it you know it" things, and may best be seen in lead V4. You should also keep in mind that BER does not show rapid progression like STEMI or pericarditis, but this does not mean it is a static representation. Patients may have a dynamic 12-lead with responses in autonomic tone such as: diminishing with increased sympathetic tone/exercise/tachycardia or increasing when the heart rate slows. Also, ST elevation may gradually disappear with age.
Pericarditis can present similar to BER, but there are very key things to keep in mind while differentiating between the two. Here are two side by sides of BER and Pericarditis.
BER indicators:
• ST elevation limited to the precordial leads
• Absence of PR depression
• Prominent T waves
• ST segment/T wave ratio <0.25
• Characteristic "fish hook" in v4
• ECG changes usually stable over time
Pericarditis indicators:
• Generalized ST elevation
• Presence of PR depression
• Normal T wave amplitude
• ST segment/T wave ratio >0.25
• Absence of "fish hook" appearance in v4
• ECG slowly evolves over time
But wait a minute you said? I know, I know. Let's actually talk about Pericarditis now. Pericarditis is the inflammation of the pericardium (usually following viral infection) that produces characteristic chest pain. Chest pain that is retrosternal, pleuritic, worse while lying flat, but relieved by sitting forward. These patients will also present with tachycardia and dyspnea. There may also be an associated pericardial friction rub, or evidence of a pericardial effusion. Widespread ST elevation segment changes occur due to involvement of the underlying epicardium. Unlike BER, pericarditis evolves. There are four stages of it's evolution:
• Stage 1: wide-spread ST elevation/PR depression with reciprocal changes in aVR(first two weeks)
• Stage 2: normalization of ST changes; generalized T wave flattening (1 to 3 weeks)
• Stage 3: flattened T waves become inverted (3 to several weeks)
• Stage 4: ECG returns to normal (several weeks onwards)
Keep in mind that less than 50% of patients progress through all four classical stages. Remember, everyone is dynamic.
Some causes of pericarditis are:
• Infections- mainly viral. Sometimes bacterial, fungal, or tuberculosis
• Immunological
• Uremia
• Post-myocardial infarction/Dressler's syndrome
• Paraneoplastic syndromes
• Drug induced
• Post radiotherapy
ECG changes of acute pericarditis include:
• Widespread concave ST elevation and PR depression is present throughout precordial (v2-v6) and limb leads (I, II, aVL, aVF).
• Reciprocal ST depression and PR elevation in aVR.
• Sinus tachycardia
Pericarditis vs STEMI:
• Pericarditis can cause localized ST elevation, but there should be no reciprocal ST depression (except in aVR and V1)
• STEMI, like pericarditis, can also cause concave up ST elevation
• Only STEMI causes convex UP or horizontal ST elevation
• ST elevation greater in III than II strongly suggests STEMI
• PR segment depression is only reliably seen in viral pericarditis, not by other causes. It is often only an early transient phenomenon. MI can also cause PR segment depression too due to atrial infarction (or PR segment elevation in aVR)
• You can't rely on history either _ STEMI can also cause positional or pleuritic pain. A pericardial friction rub.
Key steps to distinguishing from STEMI:
1. Is there ST depression in a lead other than aVR or v1? STEMI
2. Is there convex UP or horizontal ST elevation? STEMI
3. Is there ST elevation greater in III than II? STEMI
4. Now look for PR depression in multiple leads, this suggests pericarditis (especially if there is a friction rub).
Next we will discuss left ventricular hypertrophy (LVH). LVH is when the left ventricle is constantly pumping against increased resistance (chronic hypertension, aortic stenosis), the muscle hypertrophies like any other muscle. The thickened muscle wall takes longer to depolarize and longer to repolarize. All of this results in increased R-wave amplitude in the left sided leads (I, aVL, V4-V6) and increased S-wave depth in the right sided leads (III, aVR, V1-V3). Repolarization abnormalities can cause ST segment depressions and T-wave inversions in the lateral leads, known as the left ventricular strain pattern. Here is some voltage criteria for LVH.
Limb Leads (I, II, III, aVL, aVF, aVR):
• R wave in lead 1+ S wave in lead III >25mm
• R wave in aVL > 11mm
• R wave in aVF >20mm
• S wave in aVR > 14mm
Precordial Leads (v1-v6):
• R wave in v4, v5, or v6 >26mm
• Largest R wave + largest S wave in percordial leads >45mm
• R wave in v5 or v6 +S wave in v1 >35mm (most frequently used criteria known as Sokolow-Lyon criteria)
Another criteria that is less well-known, however more accurate is the Cornell-criterion:
• R in aVL + S in v3 >28mm in men
• R in aVL + S in v3 >10mm in women
Well shit, you found yourself some LVH, but how do you know this is LVH with strain or a STEMI? Following I will add a diagram of a flow chart that Armstrong et al introduced to help identify a STEMI in patients with LVH.
So there you have it. There are other imposters out there such as Brugada syndrome, and certain electrolyte deficiencies. So continue your arsenal of knowledge to continue helping your patients in the most effective manner possible. Also, not all calls are "bullshit". If a patient has any co-morbidity then they are worth your full attention. Because if you are transporting them now in the early stages of there disease/illness, then the chances of you transporting them later on at a life-threatening time is increased. Keep that in mind and do a full assessment, regardless of the nature of the incident. You will learn, and understand the progression of death. Thank you for your interest in this topic. As I learn a style of writing that keeps people engaged I will continue to do this.