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Chapter 10 - 12 lead Interpretation - Part 2
- 1. ONTARIO BASE HOSPITALGROUP Chapter 10 for 12 Lead Training -12 Lead Interpretation – Part 2- Ontario Base Hospital Group Education Subcommittee 2008 TIME IS MUSCLE
- 2. 12 Lead Interpretation– Part 2 REVIEWERS/CONTRIBUTORS Neil Freckleton, AEMCA, ACP Hamilton Base Hospital Jim Scott, AEMCA, PCP Sault Area Hospital Ed Ouston, AEMCA, ACP Ottawa Base Hospital Laura McCleary, AEMCA, ACP SOCPC Tim Dodd, AEMCA, ACP Hamilton Base Hospital Dr. Rick Verbeek, Medical Director OBHG Education Subcommittee AUTHOR Greg Soto, BEd, BA, ACP Niagara Base Hospital 2008 Ontario Base Hospital Group SOCPC
- 3. Chapter 10 -Objectives Recognize ST-depression and relate to the ACS patient Recognize Reciprocal Changes (RCs) and relate to the significance of STEMI Recognized Q-waves and relate to the ACS patient Discuss the evolution of an AMI Explain the reasons why a normal ECG does not rule out AMI OBHG Education Subcommittee
- 4. Ischemia Epicardial CoronaryArtery Thrombus forming Lateral Wall of LV Positive Electrode OBHG Education Subcommittee Septum Left Ventricular Cavity Inferior Wall of LV
- 5. OBHG Education Subcommittee Ischemia Inadequate oxygen to tissue Subendocardial Represented by ST depression or T-wave inversion May or may not result in infarct
- 6. OBHG Education Subcommittee ST depression
- 7. T-wave Inversion OBHGEducation Subcommittee
- 8. OBHG Education Subcommittee Evolution of AMI • HHyyppeerraaccuuttee TT WWaavvee
- 9. OBHG Education Subcommittee Evolution of AMI • AAccuuttee
- 10. OBHG Education Subcommittee Evolution of AMI • AAccuuttee
- 11. OBHG Education Subcommittee Evolution of AMI • AAggee uunnddeetteerrmmiinneedd
- 12. Hyper-acute T-waves OBHGEducation Subcommittee Earliest ECG sign of AMI Tall and peaked w/in minutes of blood flow interruption Differential Dx: hyperkalemia BER LVH
- 13. Why hyper-acute T-waveare OBHG Education Subcommittee important to recognize
- 14. OBHG Education Subcommittee AMI Recognition A “normal” 12-lead ECG DOES NOT rule out AMI Not all AMI have STE (approx. 50%) Early AMI may have no STE but may evolve over time Non STEMI AMI have non specific but abnormal ECGs
- 15. Why can’t AMIbe ruled out? PHECG has high specificity for STEMI = 97%* Meaning = when PHECG shows STEMI it almost always turns out to be an AMI. OBHG Education Subcommittee
- 16. Why can’t AMIbe ruled out? PHECG has only moderate sensitivity for AMI = 68% Meaning - when PHECG does not show STEMI only 68% of time does it turn out to NOT be an AMI. (over 30% of AMI patients do not have STE on PHECG) CAN’T RULE OUT AMI WITH NO STE OBHG Education Subcommittee on 12 LEAD ECG Source: Ioannides JA et al. Accuracy & clinical effect of out-of-hospital ECG in the diagnosis of acute cardiac ischemia: a meta-analysis. Annals of Emergency Medicine 2001;37.
- 17. OBHG Education Subcommittee Practice
- 18. OBHG Education Subcommittee Practice
- 19. OBHG Education Subcommittee Practice
- 20. OBHG Education Subcommittee QRS Q waves Physiologic Q waves < .04 sec (40ms) Pathologic Q waves >.04 sec (40 ms)
- 21. OBHG Education Subcommittee Q-wave & Infarct represent irreversible necrosis – death of tissue may develop early (1st hour) but usually 8-12 hours post-AMI may persist permanently but some resolve regardless of reperfusion not all AMIs produce Q-waves
- 22. OBHG Education Subcommittee QRS Q wave
- 23. OBHG Education Subcommittee QS Complex
- 24. Common Q-waves “ageundetermined” Likely old septal MI ↑ index of suspicion not a bad idea Q-wave associated with an AMI = necrosis has likely begun ↑↑ sseevveerriittyy//sseerriioouussnneessss OBHG Education Subcommittee
- 25. ONTARIO BASE HOSPITALGROUP Sample ECGs with Q-waves Find them……….
- 26. OBHG Education Subcommittee Septal – V1 to V3 (? – II, III, aVF )
- 27. OBHG Education Subcommittee Lateral - aVL
- 28. OBHG Education Subcommittee aVL, V1 – V5
- 29. ONTARIO BASE HOSPITALGROUP Reciprocal Changes
- 30. Reciprocal Changes OBHGEducation Subcommittee Occur in larger MI Able to “see” the MI on the opposite side because it is larger RC’s make the STE more likely to be due to AMI Don’t have to have RC’s but they make the diagnosis easier
- 31. Reciprocal Changes OBHGEducation Subcommittee
- 32. Reciprocal Changes OBHGEducation Subcommittee
- 33. Reciprocal Changes IIII,,IIIIII,, aaVVFF II,, aaVVLL,, VV lleeaaddss OBHG Education Subcommittee
- 34. Reciprocal Changes OBHGEducation Subcommittee Inferior Anterior = Septal, Anterior and Lateral walls
- 35. OBHG Education Subcommittee Practice
- 36. OBHG Education Subcommittee Practice
- 37. OBHG Education Subcommittee AMI Recognition
- 38. OBHG Education Subcommittee AMI Recognition Imitators of infarct BBB LVH Ventricular beats Pericarditis Early Repolarization Others
- 39. OBHG Education Subcommittee Summary AMI recognition Know what you are looking for > 1mm of ST elevation in limb leads > 2mm of ST elevation in chest leads Two contiguous leads Know where you are looking Positive electrode as an “eye” Memorize lead locations
- 40. OBHG Education Subcommittee Summary Reciprocal Changes Not necessary to presume infarction Strong confirming evidence when present
- 41. OBHG Education Subcommittee Summary ST segment elevation is presumptive evidence for AMI Other conditions may also cause ST elevation
- 42. OBHG Education Subcommittee Summary NEVER FORGET: A normal 12-Lead ECG DOES NOT rule out AMI
- 43. ONTARIO BASE HOSPITALGROUP QUESTIONS?
- 44. ONTARIO BASE HOSPITALGROUP Well Done! Education Subcommittee START QUIT
Editor's Notes
- #5 &lt;number&gt; The vessel lumen is now narrowed by a clot. If the clot is incomplete or collateral circulation is good, only the hardworking, poorly perfused sub-endocardial tissue will become ischemic. This is represented on the ECG by ST depression or T wave inversion.
- #6 &lt;number&gt; Define ischemia. Inadequate oxygen to tissue. SUBENDOCARDIAL DEFINED Represented by ST depression or T inversion. May or may not result in infarct (duration of clot and demand). If infarct develops, may or may not display Q wave. The direction of ST deviation is a poor predictor of Q wave development.
- #7 &lt;number&gt; Note widespread ST depression and T waves inverted in several leads.
- #8 T-wave inversion, same as ST-depression = ischemia. They are thought of as one and same.
- #9 &lt;number&gt; While ST segment elevation is presumptive evidence of an AMI, there is a whole spectrum of ECG changes associated with AMI. If one were to monitor the heart as a coronary artery became occluded, the earliest ECG change suggestive of AMI would be the T wave becoming tall and peaked. This is referred to as a HYPERacute change, because it may occur so early as to actually precede clinical symptoms. Of course hyperacute T waves are seen only in leads “looking” at the infarcting area. Note: True hyperacute T waves are identified not only by their height, but by their shape as well. However, participants often wonder “how tall is tall”? As a rule of thumb T wave height can normally be up to five millimeters in the limb leads and ten millimeters in the chest leads.
- #10 &lt;number&gt; ST segment elevation is the next probable ECG change. ST segment elevation implies at least three things: 1. Myocardial tissue injury is presently occurring. (NOT an old MI – it is happening right NOW) 2. This injury is probably due to an occluded coronary artery. 3. Unless corrected, this condition will lead to tissue necrosis. Therefore, even though necrosis has not yet occurred, we say that ST segment elevation is “presumptive evidence” of AMI. Final point: when the ST segment is elevated we assume that the infarct is acute rather than old.
- #11 &lt;number&gt; Note that the ST segment is elevated. We therefore assume that the infarct is acute (occurring right now). However, notice the presence of a Q wave that is at least 40 milliseconds wide. This pathologic Q wave is associated with cellular necrosis. ECG evidence now suggests that some myocardium is only injured and can still be saved (ST elevation) while some other portions of the myocardium may have already become necrotic (Q wave). It is critical to recognize and consider this pattern as acute and target this patient for reperfusion therapy. NOTE: When Q waves first form, the tissue may not yet be necrotic and, with prompt reperfusion, the Q waves may disappear.
- #12 &lt;number&gt; Note the presence of a wide Q, and the absence of ST segment elevation. This ECG pattern is associated with a previous MI. It is not possible to determine when this infarct may have occurred, so it is described as “age undetermined” rather than “an old MI”. Look for these additional changes associated with AMI as we practice infarct recognition and localization, but remember, the most important finding is ST elevation in two contiguous leads.
- #13 The diagram above shows the general pattern of ST changes associated with AMI. The point to make for participants is that while every AMI presents slightly differently the above pattern is the most common: A = beginning rise of T wave. B = Hyper-acute T wave (first sign of impending AMI). C = ST-elevation (i.e.: injury pattern) D = Q wave begins to form indicating early stages of necrosis along with continuing pattern of ST-elevation. E = ST depression indicating the heart is still ischemic but more than likely reperfusion therapy has likely been administered with success but residual evidence (ST depression) of ischemia. F = STEMI resolved with pathological Q wave indicative of previous MI (permanent necrosis).
- #14 Figure 77-1 Hyperacute T wave of acute myocardial infarction. A, Note the broad, tall T waves in leads V3 and V4 (arrows) in this patient with chest pain and diaphoresis. These are the hyperacute T waves of early ST segment elevation myocardial infarction. The ST segment is just beginning to rise in leads V3 and V4; leads V1 and V2 are also suspicious. B, This tracing is from the same patient, roughly 10 minutes after the electrocardiogram in A. Note the prominent ST segment elevation in leads V1 to V4.
- #15 &lt;number&gt; It is critical to remember that a patient may indeed be experiencing an acute myocardial infarction even though ST segment elevation is not present on the ECG. Never make the mistake of presuming that a single 12-lead rules out AMI. Why might a 12 Lead not show ST-elevation yet an AMI be occurring? Answer: Firstly, an AMI may be unfolding in the early stages and therefore ST-elevation may not yet be showing. Medical Literature: studies of specificity and sensitivity of out-of-hospital 12 Lead ECG for AMI more likely reflect the answer.
- #16 * The source quoted shows PHECG is as good as in-hospital ECG in specificity. Lastly, NO single diagnostic test in modern emergency departments is fool-proof (100% specific & 100% sensitive) for AMI. The clinical picture, findings, risk factors and history of the patient all must be considered in determining the diagnosis of AMI.
- #17 * The source quoted shows PHECG is as good as in-hospital ECG in specificity. Lastly, NO single diagnostic test in modern emergency departments is fool-proof (100% specific & 100% sensitive) for AMI. The clinical picture, findings, risk factors and history of the patient all must be considered in determining the diagnosis of AMI.
- #18 &lt;number&gt; Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a check mark next to any lead with 1mm of ST segment elevation. Localize the area of infarction. ST↑: Leads I, aVL, V1-V6 = Extensive Anterior STEMI
- #19 &lt;number&gt; Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a check mark next to any lead with 1mm of ST segment elevation. Localize the area of infarction. Extensive anterior (septal + anterior + lateral)
- #20 &lt;number&gt; Instructions: Review the 12-lead ECG. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Compare the ST to the TP segment, looking for 1mm (one small box) of elevation (ignore ST depression for now). Place a check mark next to any lead with 1mm of ST segment elevation. Localize the area of infarction. Inferior wall infarction Note ST depression in I, AVL and V1-V3. The ask the participants to compare the elevation in aVF to the depression in aVL. Ask them if aVF elevation pattern looks similar to aVL if it were flipped upside down? Tell them there is a reason for this – it is called reciprocal changes. Lets talk about one cause of ST depression, known as reciprocal ST depression.
- #21 &lt;number&gt; Q waves can occur normally in several leads (I, III, aVL, aVF, V5, V6). These Q waves are called physiologic Q waves. Physiologic Q waves normally do not exceed 30ms. Pathology (including myocardial infarction) can place a Q wave in any lead. It is possible to examine the Q wave and, based upon its width, speculate whether it is pathologic or physiologic.
- #22 &lt;number&gt; Death of tissue. Traditionally represented by wide (equal to or greater than 40ms) Q wave. Not all infarcts develop Q waves. The direction of ST deviation (elevation or depression) is a poor predictor of Q wave development.
- #23 &lt;number&gt; When a Q wave is noted in any lead, always measure its width. Red dots indicate where the Q wave is measured. A physiologic Q wave is very narrow, usually less than 30ms (0.03 seconds). A Q wave is considered pathologic when it equals or exceeds 0.04 seconds. (one small box on the ECG grid)
- #24 &lt;number&gt; When the entire complex is negatively deflected, it is called a QS complex. The important thing to remember with QS complexes to identify them when not preceding ST-elevation is that the complex following P-wave goes DOWN before going up. A QS complex is considered equivalent to a wide Q wave. If a QS complex is found in a patient consistent with an AMI, no one calls this a QS complex. Rather it is referred to as a Q-wave.
- #25 Top ECG with V1-V3: in this particular case the infarct is thought to be old and the rule of QS applies fairly strictly. That is, slightly wide and down (QS) before up (R). In the bottom ECG (Lead II): the “Q-wave” found BEFORE STEMI is considered to be associated with this STEMI, even if there is slight up before down in complex. The rules are looser with Q-waves preceding STEMI because they represent a sign of necrosis (death of tissue) associated with AMI and should raise our heighten our concern for early reperfusion with this patient.
- #27 &lt;number&gt; Pathologic Q waves present in II, III and aVF suggest necrosis has occurred in the inferior region of the left ventricle. Some interpreters of this 12 Lead ECG may consider the tiny negative complexes preceding ST-elevation in II, III, aVF to be Q-waves. However, this would be splitting hairs – a common problem in early 12 Lead ECG interpretation with learners.
- #31 &lt;number&gt; If you see ST depression on an ECG with STE in other areas, the ST depression can be due to two things: RC’s (infarction on the opposite side) Ischemia in the area noted ST depression and R waves in lead V1 (septal) is usually an indication of a posterior MI (reciprocal changes)
- #32 &lt;number&gt; Instructions: Begin by telling participants that this is a 12 Lead ECG that indicates STEMI but it also shows signs of another finding that, when present, should heighten our sense of urgency regarding early reperfusion (i.e.: get rolling!). That finding is RECIPROCAL CHANGES. Review the 12-lead ECG with participants looking for and localizing STEMI. Go lead by lead, and pick one good complex in each lead. Find the J-point and ST segment. Localize the area of infarction. Inferior wall infarction Note ST depression in I, AVL and V1-V3. Then ask the participants to compare the elevation in aVF to the depression in aVL. Ask them if aVF elevation pattern looks similar to aVL if it were flipped upside down? Tell them there is a reason for this – it is called reciprocal changes. Lets talk about one cause of ST depression, known as reciprocal ST depression.
- #33 &lt;number&gt; We have been looking for infarct based upon the presence of ST elevation. As mentioned, not every lead is elevated when AMI is present, only the leads looking at the infarct site. In fact, those leads which look at the infarct site from the opposite perspective tend to produce the opposite changes. When a lead “sees” the AMI directly, the segment becomes elevated in that lead. However, when a lead “sees” the infarct from the opposite perspective, the ST segment may be depressed in that lead. Greg Soto comment: I have taught many 12 Lead courses to both ACPs and PCPs. The concept of reciprocal changes is often a challenge for participants to grasp. The following slides my help to establish learning this concept but be sure all participants understand it before you move on. One way to ensure this is to require all participants interpreting 12 Lead ECG in exercises note RCs when present.
- #34 &lt;number&gt; Because of the way the leads are oriented on the patients body, II, III and aVF are on the bottom looking up. All the other leads are on the top, looking in. Therefore, when AMI produces elevation in II, III, and aVF, it also tends to produce depression in the opposing leads.
- #35 This provides participants with an anatomical visual reference (for visual learners) of the two “regions” of the heart as represented by INF vs. ANTERIOR. Point out the RCA descending to inferior of heart. State: IF there is an infarct in this area there will likely be ST elevation in inferior leads (I, II, aVF) (click) and if the infarct is significant enough the reciprocal changes will present as ST depressions in anterior leads (all others) (click). Then describe the reverse while again pointing to areas indicated on slide. Lastly, click for the horizontal bar to appear and at this time emphasize that when present reciprocal changes should make us think about the separation of the heart into top and bottom or anterior and inferior regions.
- #36 &lt;number&gt; Instructions: Determine which leads show ST elevation. Which leads show ST depression. Localize the area of infarction. Determine if a reciprocal pattern exists. ST elevation exists in II, III and aVF. ST depression in I and aVL Does it fit the reciprocal pattern? Yes. NOTE: Not every lead on each side of the seesaw must be elevated or depressed in order to assume reciprocal changes. Rather it is more a matter of at least some leads on one end of the seesaw being elevated and some being depressed.
- #37 &lt;number&gt; Instructions: Determine which leads show ST elevation. Which show ST depression. Localize the area of infarction. Determine if a reciprocal pattern exists. Here the elevation is in leads I, aVL, V1-V5 And the depression is in leads II, III and aVF Extensive anterior infarction, with reciprocal depression
- #38 &lt;number&gt; Obvious ST elevation is seen in multiple leads. However, in this patient no infarct was present. This demonstrates the fact that conditions other than AMI can place ST segment elevation on the ECG. In later portions of the program we will learn to identify these conditions and discuss their significance in treatment decision making. Realize that we are still “treating” the clinical presentation. If you suspect AMI based upon clinical presentation, get a 12-lead. If that 12-lead has ST elevation the patient is a potential candidate for early reperfusion. Understand that some of the patients you think should receive immediate reperfusion may later be determined not to be infarcting at all. Don’t let that discourage you. We will address this issue in more detail later in the program.
- #39 &lt;number&gt; Here are some of the imitators that can produce ST elevation. The 12-lead computer interpretation will often identify their presence. However, THE PRESENCE OF AN IMITATOR ON THE ECG DOES NOT RULE OUT A SIMULTANEOUS MYOCARDIAL INFARCTION. Therefore, any patient with a clinical presentation suggestive of AMI and ST elevation should be rapidly evaluated for early reperfusion therapy. In other words, take care to avoid the mistake of mentally ruling out infarct based upon the presence of an imitator. Imitators as well as other issues relevant to prehospital 12 Lead ECG interpretation are discussed in the Confounders and other troublesome stuff chapter.
- #40 &lt;number&gt;
- #41 &lt;number&gt; RC’s make STEMI more likely also narrow QRS – not BBB and shape of ST elevation (concave vs convex)
- #42 &lt;number&gt; When clinical presentation suggests AMI and the 12-lead shows ST segment elevation, proceed as if the patient were infarcting. However, providers must be aware that there may be ST segment elevations and may not be diagnosed with AMI.
- #43 &lt;number&gt; A patient may indeed be experiencing an acute myocardial infarction even when ST segment elevation is not present on the ECG. Never make the mistake of presuming that a single 12-lead rules out AMI.