12-lead interpretation is an area many students often struggle with. While rhythm interpretation may be challenging, pattern recognition is generally enough to get by. 12-leads, however, are a different animal entirely. They are subtle, and provide a much more global picture of cardiac electrophysiology than does a 6 second rhythm strip. Interpreting 12-leads is a key skill to master, as early recognition of cardiac ischemia, can literally save a life. The adage “time is myocardium” is not an exaggeration. If caught early enough, there is often a very positive outcome for a patient suffering from a myocardial infarction. For the purposes of this guide, I want to review the following:
How to read a 12-lead
What areas the different leads correlate to in the heart
STEMI recognition and reciprocal changes
Basic 12-lead structure:
A 12-lead ECG is similar to a rhythm strip in that it provides a printout of the electrical activity in the heart. The major difference is that a rhythm strip only shows electrical activity in a single lead (lead II), which only represents the flow of electricity from one angle. In order to fully understand what I mean, we need to briefly review the cardiac conduction system.
In a healthy heart, the initial impulse to trigger depolarization of cardiac myocytes originates at the SA node. This is a bundle of specialized cells located in the right atrium. The signal generated then travels to the AV node, down the left and right bundles, and to the Purkinje fibres. When this functions properly we get a Normal Sinus Rhythm. The electrical system of the heart is made up of specialized cardiac cells that are supplied with oxygen by the Left and Right coronary artery (LCA and RCA) and their branches the left circumflex (LCX) and left anterior descending artery (LAD). In order for the electrical system to function properly, and for the myocardium to contract, blood flow through these arteries must be sufficient. If there is partial occlusion, as seen in angina, and NSTEMI, we get impaired cardiac function. If there is complete occlusion anywhere, we get a STEMI. STEMI, or an ST-segment Elevation Myocardial Infarction, is a total blockage in one or more coronary arteries. When this happens, the cells distal to the occlusion become ischemic and, if a correction is not made, necrotic. Once myocardial cells die, they stay that way. This is why time is so critical, and why we need to be able to identify a STEMI early. So lets get into how to do that.
ECG interpretation:
Just like with a rhythm strip, the 12-lead is laid out with a series of boxes. There are 5 small boxes grouped into each larger box. Horizontally, each small box represents 0.04 seconds, and vertically each small box represents 0.01mV. This should be familiar to anyone who has practiced rhythm interpretation. Unlike a rhythm strip, which only represents lead II, a 12-lead shows us the following leads:
Lead I Lateral
Lead II Right Inferior
Lead III Right Inferior
aVR Generally Augmented Limb Lead Right Arm
aVL Augmented Limb Lead Left Arm. Lateral
aVF Augmented Limb Lead Feet. Right Inferior
L1 Septal
L2 Septal
L3 Anterior
L4 Anterior
L5 Lateral
L6 Lateral
Each lead is positioned in such a way that it looks at the heart from a different angle, and thus each area is perfused by a different part of the coronary vasculature. For the purpose of ease there is a chart.
As you can see, each of the leads represents an area supplied by a specific artery. So, when we look at a 12 lead, we are attempting to determine if there is adequate perfusion to these areas, to allow for proper cardiac function. We may also be looking for electrical abnormalities that are causing an arrhythmia, or for electrolyte disturbances. However, these are not our primary use for the 12-lead ECG, which is generally performed when we are concerned about potential cardiac ischemia.
So, what exactly are we looking for?
Well, there are a few things we need to watch for in the ECG of a patient with potential ischemia. Lets talk about the changes you can expect to find. When cardiac cells are damaged, electricity flows abnormally through and around them. Where we see this abnormal conduction is in the ST-Segment of the cardiac cycle.
The ST segment begins at the end of the QRS (The S wave) and ends at the point where deflection, either upward or downward, begins the T-wave. In a normal ECG tracing, the ST segment is flat and is in line with the PR segment (the isoelectric line). When myocardial ischemia occurs, the initial damage to the cells produces ST-Segment depression. This is indicated by an ST-Segment that drops below the isoelectric line. This is a red flag, because it does indicate impaired coronary blood flow. If the blockage evolves and there is complete occlusion of the affected artery, cellular death occurs. This presents on the ECG as ST-Segment elevation. Meaning that the ST-Segment rises above the isoelectric line. It is important to note, that these changes don’t usually happen in isolation, so you will likely have depression and elevation occurring in different leads. This is because damage in one area of the heart, generally affects other areas as well. We call these other changes, reciprocal changes. We often use look for reciprocal changes to confirm our suspicion of STEMI, especially when we are unsure. There are several STEMI Mimics, such as Left Bundle Branch Blocks, Hyperkalemia, and others, that we need to be wary of before activating a cath lab. That being said, I will cover those at a later time. We have specific criteria that are designed to cut down on false positive STEMI in the field. What we are looking for are patients with the following criteria:
Chest pain, or equivalent symptoms (discomfort, burning, heaviness, pressure, etc).
Less than 12 hours from the time of pain onset (Utilize a fibrinolytic screener on those outside this window).
2mm STE in at least 2 leads v1-v3
1mm STE in ANY 2 anatomically contiguous leads
If the patient meets the above criteria, we want to call the cath lab and activate the STEMI team. I would be lying if I said it is really that simple though. Many times a STEMI will be far less obvious. 1/3 of patients having an MI do not have chest pain, and sometimes they have not evolved all the way to a STEMI. So how do we catch the ones that are high risk? The same way we do everything in EMS, we look for TRENDS. In this case we are looking for DYNAMIC CHANGES in the ECG through repeat 12-leads. If, for example, we have a patient who has constant chest pressure, exertional dyspnea, and is diaphoretic (all very obvious MI symptoms), but we don’t see elevation on the 12-lead, we can still treat with ASA, and Nitro, and then we want to REPEAT THE 12-LEAD. At a minimum the 12-lead should be done within 10 minutes of patient contact, prior to leaving the scene, and upon arrival at your destination. I would go further and say that if you are concerned, you should be doing a couple more throughout transport. Often these patients will begin to show clear changes between each 12-lead. A normal 12-lead may begin to show depression, then T-wave inversion, then eventually elevation. There may also be situations where you only have elevation in a single lead, and it may not be sufficient to meet the “official” STEMI criteria. In this case I would urge you to repeat the 12-lead often (maybe even every 5-10 minutes), and contact the cardiologist for an opinion. I may get heat for this but, it is always better to activate the cath lab for a false STEMI than it is to lose a patient because you were unsure.
So, that is a basic explanation of ST-Elevation and its evolution. As I said before, there are many other mimics, and causes of elevation, however, we need to be able to recognize it in the setting of cardiac ischemia. 12-lead interpretation is more art than any other part of paramedicine, and it takes work. I stronly advise taking every opportunity you get to look at 12-leads and get comfortable with them.
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