EKGs The Basics for FP Residents

1. EKGs�The Basics for FP Residents Jess Fogler, MD University of California, San Francisco

2. Part II Hypertrophy Ischemia Misc.

3. Train your eyes Train your eyes for Rate: Check the computer Train your eyes for Rhythm: Check the rhythm strip Check I, II, avF Train your eyes for Axis: Check I, II Train your eyes for Intervals: PR: check II QT: check the computer QRS: check I, V1

4. Hypertrophy Ischemia Misc.

5. Hypertrophy Get a cheat sheet and use it! Read the computer�it�s good at measuring things!

6. Left Ventricular Hypertrophy An approach: 1. Start with aVL: R aVL>9mmwomen or 11mmmen 2. Then look at V3: R aVL + S V3 >20mmwomen or 25mmmen You probably have your own way of diagnosing LVH (and the computer tends to be pretty acurate at diagnosing it) but just in case you don�t have a favorite set of criteria you can you these. There are over 50 criteria to diagnose LVH but these four will usually get you the diagnosis. Remember that EKG is not a great way to diagnose LVH because all the best criteria are only 20-40% sensitive but they 95% specific and if you can diagnose LVH you may be able to explain the presence of ST-T changes that otherwise might be worrisome - start at top and go down - any one of these diagnoses LVH 2. Cornell voltage 3. Sokolow-Lyon criteria 4. Romhilt-Estes You probably have your own way of diagnosing LVH (and the computer tends to be pretty acurate at diagnosing it) but just in case you don�t have a favorite set of criteria you can you these. There are over 50 criteria to diagnose LVH but these four will usually get you the diagnosis. Remember that EKG is not a great way to diagnose LVH because all the best criteria are only 20-40% sensitive but they 95% specific and if you can diagnose LVH you may be able to explain the presence of ST-T changes that otherwise might be worrisome - start at top and go down - any one of these diagnoses LVH 2. Cornell voltage 3. Sokolow-Lyon criteria 4. Romhilt-Estes

7. Left Ventricular Hypertrophy LVH with strain ST and T opposite to main QRS in all leads Except in transitional leads! Asymmetric sloping of ST segment Starts subtly with T wave flattening You probably have your own way of diagnosing LVH but in your syllabus I�ve included a set of four criteria which I find useful that you can keep for reference if you like. � So let�s talk about LVH with ST segment and T wave abnormalities otherwise known as the strain pattern? This is seen with advanced LVH and generally indicates a twofold increased risk of all-cause cardiac mortality. � In classic stain you get what some people call the �hockey puck abnormality� with it�s characteristic downward sloping ST depression in leads with dominant R waves. But actually strain pattern starts subtly with T wave flattening and evolves over time into T wave inversion which finally pulls the ST segment down with it. �As I mentioned earlier, what you see on an EKG is dominated by activity on the left side of the heart, so when there�s a problem on the left side, such as in LVH, you should see this abnormality reflected in all leads. In LVH with strain, this means that the ST segment and T wave will be directed opposite to the main direction of the QRS in all leads. So leads with dominant R waves will get ST segment depression and T wave inversion, and leads with dominant S waves will get ST elevation with upright T waves. However these rules don�t apply to the transitional leads. � When LVH is very advanced, the long transit time through the heart muscle starts to make the QRS widen slightly, and if you see this you need apply more stringent criteria in diagnosing MI, making the definition for a pathologic Q wave 40 msec instead of 30 msec. You probably have your own way of diagnosing LVH but in your syllabus I�ve included a set of four criteria which I find useful that you can keep for reference if you like. � So let�s talk about LVH with ST segment and T wave abnormalities otherwise known as the strain pattern? This is seen with advanced LVH and generally indicates a twofold increased risk of all-cause cardiac mortality. � In classic stain you get what some people call the �hockey puck abnormality� with it�s characteristic downward sloping ST depression in leads with dominant R waves. But actually strain pattern starts subtly with T wave flattening and evolves over time into T wave inversion which finally pulls the ST segment down with it. �As I mentioned earlier, what you see on an EKG is dominated by activity on the left side of the heart, so when there�s a problem on the left side, such as in LVH, you should see this abnormality reflected in all leads. In LVH with strain, this means that the ST segment and T wave will be directed opposite to the main direction of the QRS in all leads. So leads with dominant R waves will get ST segment depression and T wave inversion, and leads with dominant S waves will get ST elevation with upright T waves. However these rules don�t apply to the transitional leads. � When LVH is very advanced, the long transit time through the heart muscle starts to make the QRS widen slightly, and if you see this you need apply more stringent criteria in diagnosing MI, making the definition for a pathologic Q wave 40 msec instead of 30 msec.

8. 45 secs Take a few moments to look at this one�. � OK, I put this here to keep you on your toes and if you saw the ST depressions and were thinking about ischemia that�s good, but this is actually LVH with strain pattern, � This is just a reminder that there are many causes of ST and T wave abnormlities, and that following an orderly way of reading an EKG, especially an order which allows you to examine the intervals and look for hypertrophy before attempting to diagnose ischemia will keep you out of trouble. 9: LVH with strain Sinus rhthym LAE, RAE LVH with strain RVH (by RAE)45 secs Take a few moments to look at this one�. � OK, I put this here to keep you on your toes and if you saw the ST depressions and were thinking about ischemia that�s good, but this is actually LVH with strain pattern, � This is just a reminder that there are many causes of ST and T wave abnormlities, and that following an orderly way of reading an EKG, especially an order which allows you to examine the intervals and look for hypertrophy before attempting to diagnose ischemia will keep you out of trouble. 9: LVH with strain Sinus rhthym LAE, RAE LVH with strain RVH (by RAE)

9. Train your eyes Train your eyes for LVH: Look at�in order avL V3 Read the computer Check your cheat sheet

10. Hypertrophy Ischemia Misc.

11. Myocardial Ischemia/Infarction Anatomy: 3 main coronary arteries RCA: RV and inferior portion of LV LAD: ventricular septum and most of LV free wall LCx: lateral wall, posterior LV Anatomy: Coronary arteries lie along the epicardial surface of the heart Penetrating branches feed the heart muscle Ischemia first appears in the subendocardial region Farthest from blood supply Closest to high pressure of ventricle Extends to subepicardium (transmural)Anatomy: Coronary arteries lie along the epicardial surface of the heart Penetrating branches feed the heart muscle Ischemia first appears in the subendocardial region Farthest from blood supply Closest to high pressure of ventricle Extends to subepicardium (transmural)

12. Evolution of EKG Changes Ischemia: Prolonged QT Tall T waves T wave inversion Injury: Subendocardial: ST depression Subepicardial/transmural: ST elevation When the heart muscle is deprived of oxygen, changes in the EKG proceed in an orderly and predictable fashion. When myocardial cells are first deprived of oxygen, they become ischemic. The cells remain intact and conduct the QRS normally, but you can think of them as being stunned stunned and slow to respond and the main effects are seen during repolarization where there can be prolonging of the QT interval, and changes in the T waves ranging from tall T waves to inverted T waves. As the heart continues to be deprived of oxygen the cells become injured and cellular ion channels are disrupted. This leads to production a current during the ST segment when normally there is none and can be seen on the EKG as either ST depression or ST elevation. Injury first appears in the subendocardial region because it is farthest from the blood supply and closest to the high pressure of the ventricle. As the supply of oxygen continues to be disrupted, the injury will then spread to the subepicardium and become transmural, or full-thickness. � When the heart muscle is deprived of oxygen, changes in the EKG proceed in an orderly and predictable fashion. When myocardial cells are first deprived of oxygen, they become ischemic. The cells remain intact and conduct the QRS normally, but you can think of them as being stunned stunned and slow to respond and the main effects are seen during repolarization where there can be prolonging of the QT interval, and changes in the T waves ranging from tall T waves to inverted T waves. As the heart continues to be deprived of oxygen the cells become injured and cellular ion channels are disrupted. This leads to production a current during the ST segment when normally there is none and can be seen on the EKG as either ST depression or ST elevation. Injury first appears in the subendocardial region because it is farthest from the blood supply and closest to the high pressure of the ventricle. As the supply of oxygen continues to be disrupted, the injury will then spread to the subepicardium and become transmural, or full-thickness. �

13. Injury currents are normally directed away from the surface that is injured. So, when there injury is limited to the subendocardium, there will be a current directed away from the endocardial surface, that is to say, towards the middle of the heart and this will be seen as ST depression by leads viewing the outer surface of that area. Injury currents are normally directed away from the surface that is injured. So, when there injury is limited to the subendocardium, there will be a current directed away from the endocardial surface, that is to say, towards the middle of the heart and this will be seen as ST depression by leads viewing the outer surface of that area.

14. On the other hand, when injury becomes full-thickness, the current will be directed away from the epicardial surface, that is to say, outward from the heart, and this will be seen as ST segment elevation by leads that view the injured surface of the heart. �animation� Also, leads that view the opposite side of the heart may see the current as ST depression and this is what is known as reciprocal change. Reciprocal changes are only seen in full-thickness injury, presumably because you need a pretty big disruption to be viewed through several layers of normal myocardiumOn the other hand, when injury becomes full-thickness, the current will be directed away from the epicardial surface, that is to say, outward from the heart, and this will be seen as ST segment elevation by leads that view the injured surface of the heart. �animation� Also, leads that view the opposite side of the heart may see the current as ST depression and this is what is known as reciprocal change. Reciprocal changes are only seen in full-thickness injury, presumably because you need a pretty big disruption to be viewed through several layers of normal myocardium

15. Evolution of EKG Changes Infarct: Pathologic Q waves Later, inverted T waves Over time: Q�s can be lost 30% lost in 3 months ST segment elevation resolves T wave inversion may or may not persist Nonspecific ST-T abnormalities As the insult progresses the myocardial cells die and become unable to conduct impulses. The depolarization of the ventricle has to travel around and away from the injured area and we begin to see morphologic changes in the QRS segment, most commonly pathologic Q waves which can appear immediately and are often maximal by 10 hours. � Usually, during this acute phase you will also see continued ST segment elevation and possibly the beginning of T wave inversion. (you can refer back to EKG #2 in your syllabus for a great example of this) A fully evolved infarct will have Q waves, an ST segment which may retain a slight convex upward shape, and inverted T waves. � Over time, - Q waves can be lost (in fact at rate of up to 30% in 3 months) the ST segment elevation usually improves, and if it doesn�t this implies dyskinetic wall motion, and often ventricular aneurysm and the T waves inversion may or may not persist. Frequently what you�re left with is the ubiquitous non-specific ST-T abnormalities. � Ok, so just a quick word about T wave inversion. You�ll recall that T wave inversion may be one of the earliest signs of ischemia, before ST elevation or Q waves appear. You�ll also notice that T wave inversion may be the only thing left after an infarct has evolved and the Q waves have disappeared and the ST segment has normalized. So, how do you know the difference? You don�t. You�ll need to look at the clinical scenario and fall back on your excellent history-taking skills to guide your management, and of course having an old EKG to compare to the current one, can be indispensable. As the insult progresses the myocardial cells die and become unable to conduct impulses. The depolarization of the ventricle has to travel around and away from the injured area and we begin to see morphologic changes in the QRS segment, most commonly pathologic Q waves which can appear immediately and are often maximal by 10 hours. � Usually, during this acute phase you will also see continued ST segment elevation and possibly the beginning of T wave inversion. (you can refer back to EKG #2 in your syllabus for a great example of this) A fully evolved infarct will have Q waves, an ST segment which may retain a slight convex upward shape, and inverted T waves. � Over time, - Q waves can be lost (in fact at rate of up to 30% in 3 months) the ST segment elevation usually improves, and if it doesn�t this implies dyskinetic wall motion, and often ventricular aneurysm and the T waves inversion may or may not persist. Frequently what you�re left with is the ubiquitous non-specific ST-T abnormalities. � Ok, so just a quick word about T wave inversion. You�ll recall that T wave inversion may be one of the earliest signs of ischemia, before ST elevation or Q waves appear. You�ll also notice that T wave inversion may be the only thing left after an infarct has evolved and the Q waves have disappeared and the ST segment has normalized. So, how do you know the difference? You don�t. You�ll need to look at the clinical scenario and fall back on your excellent history-taking skills to guide your management, and of course having an old EKG to compare to the current one, can be indispensable.

16. EKG Diagnosis of MI How sensitive is the EKG for diagnosis of MI? Multicenter Chest Pain Study: prospective study of 1024 pts with documented MI: Rouan et al. Am J Cardiol (1989) So, how good is the EKG at detecting MI�s? This is a summary of the results from the multicenter chest pain study done in 1989 by Rouan. They looked at over 1000 patient who were admitted through the ER and were then confirmed to have had an MI. They then went back to the initial EKG from the ER and looked for EKG abnormalities suggestive of the MI. Overall 93% of patients had some type of EKG abnormality. But only 45% of them had classic ST elevation or abnormal Q waves. 20% had significant ST depression. And reasonable number had only ST depression less than 1mm or non-specific ST-T changes. Also, 3% had a normal EKG. � This just serves as a reminder that the EKG is an imperfect tool which really needs to be interpreted in the full clinical context and isn�t a substitute for your clinical judgement. That said however, the sensitivity of the EKG for classic MI changes increases with serial EKGs to 80-90% � So, how good is the EKG at detecting MI�s? This is a summary of the results from the multicenter chest pain study done in 1989 by Rouan. They looked at over 1000 patient who were admitted through the ER and were then confirmed to have had an MI. They then went back to the initial EKG from the ER and looked for EKG abnormalities suggestive of the MI. Overall 93% of patients had some type of EKG abnormality. But only 45% of them had classic ST elevation or abnormal Q waves. 20% had significant ST depression. And reasonable number had only ST depression less than 1mm or non-specific ST-T changes. Also, 3% had a normal EKG. � This just serves as a reminder that the EKG is an imperfect tool which really needs to be interpreted in the full clinical context and isn�t a substitute for your clinical judgement. That said however, the sensitivity of the EKG for classic MI changes increases with serial EKGs to 80-90% �

17. EKG Diagnosis of MI 1. Examine T waves, ST segments, QRS for signs of ischemia, injury, infarction 2. Characterize the location and the extent of the insult 3. Determine the age of the insult When you use an EKG to evaluate a patient with chest pain you are really trying to answer certain basic questions: firstly, whether or not there evidence of myocardial damage, and if so, how bad that damage is, the location of the damage and the how long ago it occurred. � This can be roughly broken down into the four step process which I�ve outlined here: � (read the steps) Let�s look at each of these steps in more detail. �When you use an EKG to evaluate a patient with chest pain you are really trying to answer certain basic questions: firstly, whether or not there evidence of myocardial damage, and if so, how bad that damage is, the location of the damage and the how long ago it occurred. � This can be roughly broken down into the four step process which I�ve outlined here: � (read the steps) Let�s look at each of these steps in more detail. �

18. EKG Diagnosis of MI 1. Look for signs of ischemia/injury T wave changes Flattening, inversion Tall T waves ST elevation indicates primary area = 1 mm in at least two anatomically contiguous leads ST depression Subendocardial injury Reciprocal change Your first step is to identify the presence of myocardial ischemia or injury by examining the ST segments and the T waves. The most worrisome finding would be ST segment elevation of at least 1mm in two continguous leads indicating actual cell injury. And if you find ST elevation, this always indicates the primary area of injury. Ischemic ST segments tend to have an upward rounded look like you see here. This is sometimes called �tombstoning�. � If you find ST segment depression this can indicate either an area of subendocardial injury or else a reciprocal change. Reciprocal changes happen in leads that are more or less opposite the injured area. So an injured anterior area may produce reciprocal changes in the inferior leads, which is what we saw in EKG #2 in your packet, or vice versa. � In any case� (hot tip)� whenever you see ST segment depression you should go on a thorough search for ST segment elevation to see whether you�re dealing with subendocardial injury or transmural injury because you need this information to determine how bad the insult is. � At this time you should also examine the T wave morphology as this is often the only sign of a problem. Your first step is to identify the presence of myocardial ischemia or injury by examining the ST segments and the T waves. The most worrisome finding would be ST segment elevation of at least 1mm in two continguous leads indicating actual cell injury. And if you find ST elevation, this always indicates the primary area of injury. Ischemic ST segments tend to have an upward rounded look like you see here. This is sometimes called �tombstoning�. � If you find ST segment depression this can indicate either an area of subendocardial injury or else a reciprocal change. Reciprocal changes happen in leads that are more or less opposite the injured area. So an injured anterior area may produce reciprocal changes in the inferior leads, which is what we saw in EKG #2 in your packet, or vice versa. � In any case� (hot tip)� whenever you see ST segment depression you should go on a thorough search for ST segment elevation to see whether you�re dealing with subendocardial injury or transmural injury because you need this information to determine how bad the insult is. � At this time you should also examine the T wave morphology as this is often the only sign of a problem.

19. EKG Diagnosis of MI Two areas of special concern: Posterior injury Will only show reciprocal changes on a standard 12 lead EKG ST depression or R waves leads V1-3 Let me point out two areas that get missed on a standard 12 lead EKG: these are the posterior portion of the LV and the right ventricle. � On a standard 12 lead EKG, posterior injury will only be seen as a reciprocal change in the anterior leads V1-3, and right ventricular injury is often missed altogether and needs right sided leads to evaluate properly Let me point out two areas that get missed on a standard 12 lead EKG: these are the posterior portion of the LV and the right ventricle. � On a standard 12 lead EKG, posterior injury will only be seen as a reciprocal change in the anterior leads V1-3, and right ventricular injury is often missed altogether and needs right sided leads to evaluate properly

20. EKG Diagnosis of MI Two areas of special concern: Right ventricle injury Best assessed with right sided leads A complication of inferior infarct (19-43%) Clinically important Best criterion: ST elevation in V4R Let me point out two areas that get missed on a standard 12 lead EKG: these are the posterior portion of the LV and the right ventricle. � On a standard 12 lead EKG, posterior injury will only be seen as a reciprocal change in the anterior leads V1-3, and right ventricular injury is often missed altogether and needs right sided leads to evaluate properly Let me point out two areas that get missed on a standard 12 lead EKG: these are the posterior portion of the LV and the right ventricle. � On a standard 12 lead EKG, posterior injury will only be seen as a reciprocal change in the anterior leads V1-3, and right ventricular injury is often missed altogether and needs right sided leads to evaluate properly

21. EKG Diagnosis of MI Examine QRS for signs of infarction �Poor R wave progression� Loss of R wave height across precordial leads Normal R wave height increases V1 - V5 with V5 > V6 The next step is to look for evidence of infarction by scanning the QRS segments for morphologic changes. � The one we all remember is to look for pathologic Q waves. A pathologic Q wave is considered to by ANY Q wave in leads V1-3, or a Q wave wider than 30 msecs (or 3/4 of a small box) in most other leads except III and avR. Lead III is excluded because there are too many false positives in this lead, and aVR is exluded because it�s upside down and will often have a normal Q wave. � Another criterion for diagnosing an infarct is the presence of a wide R wave in the anterior leads which represents posterior infarct and is essentially the equivalent of a Q wave seen reciprocally. You�d see a real Q wave if you checked posterior leads. � And then there�s always the popular term �poor R wave progression� in which there is a loss of R wave height or an interruption of the normal R wave height increase from V1-V5. But be careful in using this term because it hasn�t been well-defined and it�s not very specific for MI. The next step is to look for evidence of infarction by scanning the QRS segments for morphologic changes. � The one we all remember is to look for pathologic Q waves. A pathologic Q wave is considered to by ANY Q wave in leads V1-3, or a Q wave wider than 30 msecs (or 3/4 of a small box) in most other leads except III and avR. Lead III is excluded because there are too many false positives in this lead, and aVR is exluded because it�s upside down and will often have a normal Q wave. � Another criterion for diagnosing an infarct is the presence of a wide R wave in the anterior leads which represents posterior infarct and is essentially the equivalent of a Q wave seen reciprocally. You�d see a real Q wave if you checked posterior leads. � And then there�s always the popular term �poor R wave progression� in which there is a loss of R wave height or an interruption of the normal R wave height increase from V1-V5. But be careful in using this term because it hasn�t been well-defined and it�s not very specific for MI.

22. EKG Diagnosis of MI The next step is to look for evidence of infarction by scanning the QRS segments for morphologic changes. � The one we all remember is to look for pathologic Q waves. A pathologic Q wave is considered to by ANY Q wave in leads V1-3, or a Q wave wider than 30 msecs (or 3/4 of a small box) in most other leads except III and avR. Lead III is excluded because there are too many false positives in this lead, and aVR is exluded because it�s upside down and will often have a normal Q wave. � Another criterion for diagnosing an infarct is the presence of a wide R wave in the anterior leads which represents posterior infarct and is essentially the equivalent of a Q wave seen reciprocally. You�d see a real Q wave if you checked posterior leads. � And then there�s always the popular term �poor R wave progression� in which there is a loss of R wave height or an interruption of the normal R wave height increase from V1-V5. But be careful in using this term because it hasn�t been well-defined and it�s not very specific for MI. The next step is to look for evidence of infarction by scanning the QRS segments for morphologic changes. � The one we all remember is to look for pathologic Q waves. A pathologic Q wave is considered to by ANY Q wave in leads V1-3, or a Q wave wider than 30 msecs (or 3/4 of a small box) in most other leads except III and avR. Lead III is excluded because there are too many false positives in this lead, and aVR is exluded because it�s upside down and will often have a normal Q wave. � Another criterion for diagnosing an infarct is the presence of a wide R wave in the anterior leads which represents posterior infarct and is essentially the equivalent of a Q wave seen reciprocally. You�d see a real Q wave if you checked posterior leads. � And then there�s always the popular term �poor R wave progression� in which there is a loss of R wave height or an interruption of the normal R wave height increase from V1-V5. But be careful in using this term because it hasn�t been well-defined and it�s not very specific for MI.

23. EKG Diagnosis of MI 2. Locate the insult Anterior (39%) ST elevation in leads V1-4 Inferior (57%) ST elevation in leads II, III, aVF Apical/lateral ST elevation in leads V5-6 or I, aVL Posterior ST depression leads V1-3 (reciprocal changes) Right Ventricle ST elevation in V4R Once you�ve determined that you have a myocardial insult and you�ve assessed the severity , the next step is to better characterize the location. � This is important because both the location and the extent of the infarct will help you risk-statify the patient. For example patients with anterior injury generally have a worse outcome than patients with inferior injury, and obviously the larger the area of injury the worse the outcome. � Anterior usually is the result of a occlusion of the LAD or one of it�s branches and will be seen on an EKG as ST elevation or Q waves in leads V1-V4. � Inferior injury happens when there is occlusion of one of the branches of the RCA. On the EKG you�ll see ST elevation or Q waves in leads II, III, and F. Apical or Lateral injury is most offen an extension of anterior injury and will be seen as ST elevation or Q waves in V5-6 or I and L. � Posterior injury can happen because of occlusion of the Lcx or the RCA, depending on the anatomy and on a standard 12 Lead EKG will be seen as ST depression or wide R waves, representing a reciprocal change in leads V1-3. � (hot tip) so if you see ST depression in leads V1-3 it�s a good idea to get posterior chest leads, which are essentially just a continuation of the normal left-sided chest leads to look for ST elevation in this area. GUSTO percentagesOnce you�ve determined that you have a myocardial insult and you�ve assessed the severity , the next step is to better characterize the location. � This is important because both the location and the extent of the infarct will help you risk-statify the patient. For example patients with anterior injury generally have a worse outcome than patients with inferior injury, and obviously the larger the area of injury the worse the outcome. � Anterior usually is the result of a occlusion of the LAD or one of it�s branches and will be seen on an EKG as ST elevation or Q waves in leads V1-V4. � Inferior injury happens when there is occlusion of one of the branches of the RCA. On the EKG you�ll see ST elevation or Q waves in leads II, III, and F. Apical or Lateral injury is most offen an extension of anterior injury and will be seen as ST elevation or Q waves in V5-6 or I and L. � Posterior injury can happen because of occlusion of the Lcx or the RCA, depending on the anatomy and on a standard 12 Lead EKG will be seen as ST depression or wide R waves, representing a reciprocal change in leads V1-3. � (hot tip) so if you see ST depression in leads V1-3 it�s a good idea to get posterior chest leads, which are essentially just a continuation of the normal left-sided chest leads to look for ST elevation in this area. GUSTO percentages

24. EKG Diagnosis of MI 4. Determine the age of the insult Ischemia: T wave changes Acute injury: ST elevation and peaked T waves Acute infarct: Pathologic Q waves Inverted T waves Old infarct: Possibly Q�s Possibly T wave inversion Non-specific ST-T changes Finally you�ll combine all this information to make an estimation of how old the insult is. � To review: In the earliest ischemia there can be changes in the T waves including T wave inversion. Early acute injury will show ST elevation with tall upright T waves. � As this progresses to infact, Q waves appear and the T waves invert, � and over time, Q waves may or may not persist, the ST segment elevation resolves largely, and the T waves may be upright, flattened or remain inverted, possibly leaving �non-specific ST-T changes� Finally you�ll combine all this information to make an estimation of how old the insult is. � To review: In the earliest ischemia there can be changes in the T waves including T wave inversion. Early acute injury will show ST elevation with tall upright T waves. � As this progresses to infact, Q waves appear and the T waves invert, � and over time, Q waves may or may not persist, the ST segment elevation resolves largely, and the T waves may be upright, flattened or remain inverted, possibly leaving �non-specific ST-T changes�

25. Train your eyes Train your eyes for MI: Look at all T waves Look at all ST segments Check for Q waves Check for R waves in V1-2

26. NO TIME This is the same EKG you saw a little while ago and you can clearly see the ST segment elevations, upright T waves, and Q waves in the anterior and lateral leads, and the reciprocal changes in the inferior leads indicative of and acute anterior MI with apical and lateral extenstion. 19: Same EKG as before Acute anterior MI with apical and lateral extension. ST elevation V1-5, I,L Stdepression ii,iii,F Q�s v1-4, I,L NO TIME This is the same EKG you saw a little while ago and you can clearly see the ST segment elevations, upright T waves, and Q waves in the anterior and lateral leads, and the reciprocal changes in the inferior leads indicative of and acute anterior MI with apical and lateral extenstion. 19: Same EKG as before Acute anterior MI with apical and lateral extension. ST elevation V1-5, I,L Stdepression ii,iii,F Q�s v1-4, I,L

27. NO TIME This EKG is from the same patient as in the previous EKG only 3 days later. Here you see the ST segments are less elevated and have a rounded look to them. The T waves are biphasic or inverted in many places and the Q waves are more pronounced. You also see a loss of R wave height in all chest leads. Finally, the reciprocal changes seen in the inferior leads are now gone. 20: Same patient as previous EKG 3 days later Rounded ST elevation in V1-5 ST depression in inferior leads basically gone Q�s in V1-4, and more notable now in I,L Loss of R wave height in all precordial leads NO TIME This EKG is from the same patient as in the previous EKG only 3 days later. Here you see the ST segments are less elevated and have a rounded look to them. The T waves are biphasic or inverted in many places and the Q waves are more pronounced. You also see a loss of R wave height in all chest leads. Finally, the reciprocal changes seen in the inferior leads are now gone. 20: Same patient as previous EKG 3 days later Rounded ST elevation in V1-5 ST depression in inferior leads basically gone Q�s in V1-4, and more notable now in I,L Loss of R wave height in all precordial leads

28. Take a few moments to look at this EKG. See if you can figure out if there is an injury, how extensive it is and how old it is. If we look at the ST segments and T waves and we find flattened and inverted T waves in leads II, III,and F as well as in V5-6 and leads I and L. We also find Q waves in these leads, as well as R waves in V1-3. We can therefore conclude that this is an old inferior infarct with apical, lateral and posterior extension. And this is probably a Lcx lesion in which the LCX was dominant and fed the inferior portion of the LV. 36: Old inferior MI with apical, lateral and posterior extension Probably Lcx lesion NSR LAE LAD secondary to inf MI, LAFB Flat/flipped T�s laterally, inferiorly Q�s in II, III, F, V5-6, I, ?L R�s in V1-3 Take a few moments to look at this EKG. See if you can figure out if there is an injury, how extensive it is and how old it is. If we look at the ST segments and T waves and we find flattened and inverted T waves in leads II, III,and F as well as in V5-6 and leads I and L. We also find Q waves in these leads, as well as R waves in V1-3. We can therefore conclude that this is an old inferior infarct with apical, lateral and posterior extension. And this is probably a Lcx lesion in which the LCX was dominant and fed the inferior portion of the LV. 36: Old inferior MI with apical, lateral and posterior extension Probably Lcx lesion NSR LAE LAD secondary to inf MI, LAFB Flat/flipped T�s laterally, inferiorly Q�s in II, III, F, V5-6, I, ?L R�s in V1-3

29. Train your eyes Train your eyes for Rate: Check the computer Train your eyes for Rhythm: Check the rhythm strip Check I, II, avF Train your eyes for Axis: Check I, II Train your eyes for Intervals: PR: check II QT: check the computer QRS: check I, V1

30. Train your eyes Train your eyes for LVH: Look at�in order avL V3 Check your cheat sheet Read the computer Train your eyes for MI: Look at all T waves Look at all ST segments Check for Q waves Check for R waves in V1-2