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1. 1. 12 Lead ECG Basic Concepts By Judy Washington, CRNP
2. 2. Objectives <ul><li>1. Understand cardiac anatomy </li></ul><ul><li>2. Understand the measurements of the EKG paper </li></ul><ul><li>3. Steps in Rhythm analysis </li></ul><ul><li>4. Meaning of axis deviation </li></ul><ul><li>5. Lead placement </li></ul><ul><li>6. Understand hypertophy </li></ul>
3. 3. The two basic functions of the heart <ul><li>1. Functions: is to circulate blood throughout the body without interruption. </li></ul><ul><li>2. To adjust the flow of blood in response to many factors in the body. </li></ul>Remember that a 12 lead ECG is a tool, used in diagnosis. The main concepts here will be placed on things to help with patient Care.
4. 4.                                                                                      Human Heart
5. 6. 1.      Rate – if regular, then count the number of large squares between R waves; 1 square = 300 bpm, 2 = 150 bpm, 3 = 100 bpm, 4 = 75 bpm, 5 = 60 bpm, 6 = 50 bpm.  Each small box = 0.04 s, each large box = 5 small boxes = 0.20 s. 2.      Rhythm – is it regular? (use calipers/ruler to make sure all R-R intervals are the same); are there P waves, and are they in front of every QRS? (in sinus rhythm, P waves will be upright in lead II); are P waves all identical? 3.      Intervals          PR interval : normally 0.12 to 0.20 seconds (will not exceed a large box)       QRS interval : normally 0.04 to 0.10 seconds (no larger than half a large box)         QT interval : should be less than half the R-R interval (if HR < 100) 4.      Axis deviation – net QRS deflection should be positive in both leads I and aVF         Right axis deviation : QRS negative in I, positive in aVF          Left axis deviation : QRS positive in I, negative in aVF
6. 7. Axis Deviation: The QRS axis is the “average” direction of electrical activity during ventricular depolarization. The QRS axis may shift due to physical change in the position of the heart, chamber hypertrophy, or conduction block. QRS Axis by Inspection Method lead I positive, lead III positive = normal axis lead I negative (+/- R positive) = RIGHT axis lead III negative, lead II negative = LEFT axis
7. 8. causes of right axis deviation normal finding in children and tall thin adults right ventricular hypertrophy chronic lung disease even without pulmonary hypertension anterolateral myocardial infarction left posterior hemiblock pulmonary embolus Wolff-Parkinson-White syndrome - left sided accessory pathway atrial septal defect ventricular septal defect
8. 9. causes of left axis deviation left anterior hemiblock Q waves of inferior myocardial infarction artificial cardiac pacing emphysema hyperkalaemia Wolff-Parkinson-White syndrome - right sided accessory pathway tricuspid atresia ostium primum ASD injection of contrast into left coronary artery
9. 10. 5.      Hypertrophy         Left ventricular hypertrophy : sum of deepest S in V1 or V2 and tallest R in V5 or V6 > 35 mm (patients > 35 yo); R in aVL > 12 mm indicative of “strain”.         Left atrial enlargement : P waves are notched (M-shaped) in I, II, or aVL or a deep terminal negative component to P in V1         Right atrial enlargement : tall, peaked P waves (> 2.5 mm) in II, III, aVF          Right ventricular hypertrophy : right atrial enlargement, right axis deviation, incomplete RBBB, low voltage tall R wave in V1, persistent precordial S waves, right ventricular strain are all suggestive.
11. 12. Left atrial enlargement : P waves are notched (M-shaped) in I, II, or aVL or a deep terminal negative component to P in V1
12. 13. Right atrial enlargement : tall, peaked P waves (> 2.5 mm) in II, III, aVF
13. 14.                                                                              Right Ventricular Hypertrophy (RVH) & Right Atrial Enlargement (RAE)-KH Frank G.Yanowitz, M.D. In this case of severe pulmonary hypertension, RVH is recognized by the prominent anterior forces (tall R waves in V1-2), right axis deviation (+110 degrees), and &quot;P pulmonale&quot; (i.e., right atrial enlargement). RAE is best seen in the frontal plane leads; the P waves in lead II are >2.5mm in amplitude.
14. 15. 6.       Infarction            Q waves : small, normal Q waves can be seen in lateral leads (I, aVL, V 4 to V 6 ), while moderate-large sized Q waves may be normal in leads III, aVF, aVL, and V 1 .  To localize the infarction, look for groupings of Q waves in the following leads… Remember Infarction cover a specific region of the myocardium. V 1 and V 2 Posterior V 4 and V 6 , I, aVL Anterolateral V 3 and V 4 Anterior V 1 to V 3 Anteroseptal II, III, aVF Inferior
15. 16. ²          Q waves : small, normal Q waves can be seen in lateral leads (I, aVL, V4 to V6), while moderate-large sized Q waves may be normal in leads III, aVF, aVL, and V1.  To localize the infarction, look for groupings of Q waves in the following leads… aVF inferior III inferior V 3 anterior V 6 lateral aVL lateral II inferior V 2 septal V 5 lateral aVR I lateral V 1 septal V 4 anterior
16. 17.        R wave progression : transition should occur between V2 and V4.         ST segment elevation or depression : remember that ischemia is associated with ST depression , while infarction is associated with ST elevation.  Look for changes in two adjacent leads.          T wave inversion : may be normally inverted in III, aVF, aVL, and V1.  T wave inversion indicates areas of ischemia in Q wave infarctions. 7.         Heart Block (AV block)        1st Degree AV block: PR interval > 0.20 sec          2nd Degree AV block                                                                     i.      Mobitz I: (Wenkeback) PR interval progressively widens until a beat is dropped                                                                   ii.      Mobitz II: PR interval is prolonged, randomly dropped beatàNeeds Pacemaker       3rd Degree AV Block: No connection (dissociation) between atrial and ventricular rates Needs a Pacer
17. 18. Other pearls          Hypokalemia : ST depression, decreased or inverted T waves, U waves          Hyperkalemia : peaked T waves, decreased P waves, short QT, widened QRS, sine wave         Hypocalcemia : prolonged QT, flat or inverted T waves         Hypercalcemia : short or absent ST, decreased QTc interval          Hypomagnesemia : prolonged QT, flat T waves, prolonged PR, aFib, torsade          Hypermagnesemia : short PR, heart block, peaked T waves, widened QRS0         Digitalis toxicity : ST depression (scoop), flat T waves         Quinidine : prolonged QT, widened QRS          Pericarditis : diffuse ST elevation with PR interval depression
18. 19. New cases of LQTS are diagnosed in more female patients (60-70% of cases) than male patients. The female predominance may be related to the prolonged QTc (as determined by using the Bazett formula) in women compared with men and to a relatively high mortality rate in young men. This article for e-medicine gives examples of the information listed above and other medication that affect the QT interval.
19. 21. Distance: each small box is one millimeter, so each large box ( which contains 5 Small boxes) = 5 millimeters. Time: each small box is equivalent to 0.04 seconds, so each large box is Equivalent to 0.20 seconds. The paper runs at a standard speed of 25mm per seconds.
20. 22. There is an easier and quicker way to estimate the heart rate. As seen in the diagram below, when QRS complexes are 1 box apart the rate is 300 bpm. 2 boxes apart...150 bpm, etc. So if you memorize these simple numbers you can estimate the heart rate at a glance!
21. 29. Delta waves always occurs in the beginning of the QRS. They can look like Slurring or can take a more rounded shape. Often they encroach on the PR interval and shorten it. Delta waves are found in WPW ( Wolf-Parkinson- White) Syndrome
22. 30.
23. 31. You will notice that leads I, II and III form the sides of an equilateral triangle, while AVR, AVL and AVF bisect the vertices of the triangle.
24. 33. Hypertrophy Hypertrophy is the increase in size of the myocytes in the myocardium, leading to thicker walls. It can be non-pathological, as in the case of people who frequently perform isometric exercise (lifting heavy weights, with the straining and valsalva maneuver, produces an increased afterload). Extending this thought, we can see how hypertrophy can occur in the pathological sense by thinking about increased afterload on the heart as in individuals with high blood pressure which causes a left sided afterload increase. Left Sided afterload increases, such as systemic hypertension or aortic stenosis will cause the left ventricle (LV) to expand in response giving Left Ventricular Hypertrophy (LVH). The right side of the heart can also experience afterload. Increased pressure in the pulmonary vessels will cause an increase in afterload (back-pressure) to the right ventricle (RV), leading to an increase in muscle mass of the RV to compensate, leading to Right Ventricular Hypertrophy (RVH).
25. 35.              JAMA Patient Page: Left Ventricular Hypertrophy The major pumping chamber of the heart is the left ventricle . This heart chamber pumps oxygenated blood into the aorta , the large blood vessel that delivers blood to the body's tissues. If the left ventricle has to work too hard, its muscle hypertrophies (enlarges) and becomes thick. This is called left ventricular hypertrophy (LVH). Because of the increased thickness, blood supply to the muscle itself may become inadequate. This can lead to cardiac ischemia (not enough blood and oxygen at the tissue level), myocardial infarction (heart attack), or heart failure. The November 17, 2004, issue of JAMA includes several articles about reducing the risks of heart failure and death from LVH by treating high blood pressure.
26. 36. As the ventricles, the atria can also become hypertrophic (dilated), which is visualized as changes to the P-wave. The P-wave can become biphasic in bilateral atrial hypertrophy. The best place to look for Atrial Hypertrophy is in V1, which is mostly over the right atrium, but being the highest placed lead in the chest also gives left sided information as well). Below we see examples of Right and Left Atrial Hypertrophy showing as biphasic P-waves.                                                                                                                                     Next we need to examining the ventricles for evidence of hypertrophy there. Since increased muscle mass, logically yields to an increase in the signal (more channels -> more current) we would expect to see changes in the QRS complex morphology.
27. 37. Next we need to examining the ventricles for evidence of hypertrophy there. Since increased muscle mass, logically yields to an increase in the signal (more channels -> more current) we would expect to see changes in the QRS complex morphology. For Right Ventricular Hypertrophy we look at V1 (and less so in V2 and V3) and notice that there is a large R-wave (the normal V1 has a small R with a large S)                                 This increased R height, will taper down, in V2 and V3. Remember that just because you find RVH doesn't mean that the left ventricle is also not hypertrophied, in which case you may not see the normal taper.
28. 38. In Left Ventricular Hypertrophy (LVH), you will have a large S wave in V1 and a large R wave in V5. The actual criteria, are to add the height of S in V1 and the height of R in V5 (in mm) and if the sum is greater than 35mm, then LVH is probable. For instance in the picture below, we measure the heights (23mm in V1 and 17mm in V5) which total greater than 35mm, so we meet a criterion for LVH.
30. 42. Baseline Ischemia —tall or inverted T wave (infarct), ST segment may be depressed (angina) Injury —elevated ST segment, T wave may invert Infarction (Acute) —abnormal Q wave, ST segment may be elevated and T wave may be inverted Infarction (Age Unknown) —abnormal Q wave, ST segment and T wave returned to normal
31. 43. The R wave should grow a little in V2. It is important to look for R wave progression in the V leads. It shows that the septum is Alive and well and conducting electricity. If you don’t see an R Wave here, be suspicious of a septal infarct. Other causes of poor R wave progression include left ventricular hypertrophy, emphysema, and left bundle branch block.
32. 44. ECG Clues to the Location of Myocardial Infarction and Coronary Artery Involved. Location of Infarction ECG Leads Coronary Artery Anterior * Extensive anterior V1-V6, I, AVL Left: Left main Proximal LAD * Anteroseptal V1-V3 Left: LAD * Anterolateral V4-V6, I, AVL Left: LAD * Apical V5,V6,I, II, AVF Left: LAD (usual) Right: PDA High Lateral I, AVL Left: OMBof CFA Diagonal of LAD Inferior (diaphragramatic) II, III, AVF Right : PDA (80%) Left: CFA ( 20%) Right Ventricular Right precordial leads Right: ( Proximal) e.g. V4R, V1-V4 True Posterior Tall, broad R waves Left: CFA V1-V2(mirror image) Right: PL branch LAD- Left anterior descending; CFA= circumflex artery PDA=posterior Descending artery; OMB= obtuse marginal branch; PL=posterolateral branch
33. 45. <ul><li>Risk Factors for Coronary Artery Disease </li></ul><ul><li>Not controllable or modifiable risk factors </li></ul><ul><ul><li>Heredity </li></ul></ul><ul><ul><li>Gender </li></ul></ul><ul><ul><li>Age </li></ul></ul><ul><li>Controllable or modifiable risk factors </li></ul><ul><ul><li>Smoking </li></ul></ul><ul><ul><li>High Blood Cholesterol </li></ul></ul><ul><ul><li>High Blood Pressure </li></ul></ul><ul><ul><li>Obesity </li></ul></ul><ul><ul><li>Physical Inactivity </li></ul></ul><ul><ul><li>Stress and Behavior </li></ul></ul><ul><li>These risk factors cannot be controlled or modified: </li></ul>
34. 46. <ul><li>Other Risk Factors </li></ul><ul><li>Drug usage- Cocaine, Crack </li></ul><ul><li>Diabetes </li></ul><ul><li>Renal Failure </li></ul><ul><li>High Stress </li></ul>
35. 49. actual fluoroscopic image of blocked artery actual fluoroscopic image of blocked artery                                                                                         actual fluoroscopic image of blocked artery                                                                                         artist's rendering of same blocked artery    actual fluoroscopic image of blocked artery
36. 50. Rate: Rhythm: P waves QRS and T waves
37. 51. Rate: Rhythm Pwaves QRS & Twaves
38. 52. Rate: Rhythm P waves QRS & T waves
39. 53. Rate Rhythm P waves QRS & T waves
40. 54. Rate: Rhythm P waves QRS & T waves
41. 55. Rate Rhythm P waves QRS & T waves
42. 56. Rate Rhythm P waves QRS & T waves
43. 57. Rate Rhythm P waves QRS & T wave
44. 58. Rate Rhythm P waves QRS & T waves
45. 59. Rate Rhythm P wave QRS & T wave
46. 60. Rate Rhythm P waves QRS & T waves
47. 61. Rate Rhythm P wave QRS & T waves
48. 62. Rate Rhythm P waves QRS & T wave