1. FOCUS 1 ECG course
Dr. Boyd
SEMC

2. Part 4:
Cases and review

3. Course Objectives
To fully understand a basic approach to ECG interpretation
To recognize the 13 most common rhythm disturbances.
To recognize acute myocardial ischemia and infarction on a 12-lead ECG.

4. Course outline 1. ECG basics 2. Arrhythmias
3. Acute coronary syndromes
4. Cases and review
5. Test

5. Systematic approach R random Roy RATE R reading Rogers RHYTHM
I inhibits Is INTERVALS
A acceptable a AXIS
H heart horseback HYPERTROPHY
I interpretation icon INFARCT

6. What questions do y’all have?

7. Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

8. The ECG Paper Horizontally Vertically One small box - 0.04 s
One large box s
Vertically
One large box mV

9. The Rule of 300 It may be easiest to memorize the following table:
# of big boxes
Rate 1
300 2
150 3
100 4 75 5 60 6 50

10. 10 Second Rule
As most EKGs record 10 seconds of rhythm per page, one can simply count the number of beats present on the EKG and multiply by 6 to get the number of beats per 60 seconds.
This method works well for irregular rhythms.

11. Rhythm Summary Normal Sinus Rhythm Rate 90-95 bpm Regularity regular
P waves normal
PR interval s
QRS duration s
Interpretation?
Normal Sinus Rhythm

13. Blocks AV Blocks PR interval > 0.20 secs
(normal PR 0.12 – 0.20 secs)
Interventricular blocks
(normal QRS 0.08 – 0.10 secs)
IVCD, Incomplete BBB or Hemiblock = 0.10 –0.12 secs
BBB > 0.12 secs

14. Criteria - PR interval PR Interval 0.12 - 0.20 seconds
Delay at AV node
Protect ventricles
Allow for ventricular filling

15. Right Bundle Branch Blocks
What QRS morphology is characteristic?
For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2).
“Rabbit Ears” V1
*Many authorities define an RSR prime in V1 as “incomplete RBBB”
No matter what the QRS duration

16. Left Bundle Branch Blocks
What QRS morphology is characteristic?
For LBBB the wide QRS complex assumes a characteristic change in shape in those leads the left ventricle (right ventricular leads - V1 and V2).
Broad, deep S waves
Normal

17. What syndrome is typical of the following EKG features
What syndrome is typical of the following EKG features? -Short PR interval -Bouts of tachycardia -Upsloping R wave, “delta”wave -Often abberant conduction through ventricles (wide>0.10s QRS) -The name of this zebra is…. -Next slide for answer and EKG.

18. Lead two reveals the short PR, delta wave, and the wider-appearing QRS typical of Wolff-Parkinson-White syndrome.

19. The QT/QTc Interval: Calculation and Significance
Measurement: From the beginning of the Q wave to the end of the T wave Parameter: Normal QT intervals range from Abnormalities: Hypercalcemia will shorten the QT interval and yield measurements from s. QTc: The QT interval varies with heart rate. The corrected QT interval is calculated by adjusting your measurement for the patient’s heart rate. The QT divided by the square root of the R to R interval typically gives a QTc around 0.44 seconds. Lengthening: Diseases, drugs, and toxins can prolong the QT interval and precipitate attacks of lethal ventricular arrhythmias.

20. Long QT syndrome, “Romano-Ward” Syndrome EKG:
The QTc, adjusted for rate, would almost certainly be greater than 0.44 seconds. You can see in this example that the QTc is approximately seconds (almost 3 large boxes!)

21. The QRS Axis
By near-consensus, the normal QRS axis is defined as ranging from -30° to +90°.
-30° to -90° is referred to as a left axis deviation (LAD)
+90° to +180° is referred to as a right axis deviation (RAD)

22. Determining the Axis

23. The Quadrant Approach
1. Examine the QRS complex in leads I and aVF to determine if they are predominantly positive or predominantly negative. The combination should place the axis into one of the 4 quadrants below.

24. The Quadrant Approach
2. In the event that LAD is present, examine lead II to determine if this deviation is pathologic. If the QRS in II is predominantly positive, the LAD is non-pathologic (in other words, the axis is normal). If it is predominantly negative, it is pathologic.

25. Precise axis calculation, anyone
Precise axis calculation, anyone? Remember that it is simply a method of addition. I+III=II. The mean QRS vector will also point 90 degrees away from the most isoelectric lead. Leads with large amplitude R waves will shift the mean QRS vector in their general direction. Remember about dropping those stubborn perpendiculars?

26. Hypertrophy Right ventricular enlargement Left ventricular enlargement
Right atrial enlargement (P pulmonale)
Left atrial enlargement (P mitrale)
*P wave > 2.5 mm in height and > 0.12 seconds wide
Right ventricular enlargement
Left ventricular enlargement

27. Biphasic P waves, P waves with a terminal negative component or notched P waves are consistent with……..?

28. Left atrial enlargement
“P mitrale pattern”
Notched P wave seen in leads I and II (bigger in I than in III) with a wide, slurred diphasic P (M shaped!) in V1 with a wide terminal component (negative deflection)
The notch is greater than 0.04 sec duration
* Those that do not meet all the above criteria should be labeled Left atrial abnormality
Clinical correlations: seen with mitral stenosis or secondary to LVH

29. P mitrale

30. What about the following EKG tracing?

31. Right atrial enlargement
“P pulmonale pattern”
Tall (greater than 0.25 mv (2.5.mm)), slender, peaked P waves in II, III, and AVF (taller in III than I) with a diphasic or inverted P wave in V1
Clinical correlations: seen with COPD, pulmonary hypertension, congenital heart disease (atrial septal defects)

32. P Pulmonale

33. Right atrial enlargement: Factors suggesting right atrial enlargement include: -Tall, humped P waves -May be higher than 2.5 mm -Patient history may be significant for asthma, COPD, or pulmonary hypertension

34. Chamber enlargement review:
Name that hypertrophy?
a) RVH b) LVH c) RAH d) LAH

35. The EKG findings are consistent with: RVH
Criteria for right ventricular hypertrophy include: -Tall R wave in lead V1 (R>S) -qR pattern in V1 -Right axis deviation -T wave inversion in right to mid precordial leads possible -Commonly due to ASD! -The pattern of T wave inversion is called, “strain”and is consistent with repolarization problems in hypertrophied muscle.

36. Right ventricular hypertrophy
Tall R wave in V1 (R greater than S in V1)
S greater than R in V6
Normal QRS
Right axis deviation
ST depression, upward convex and T wave inversion V1 and V2
R’ in V1 in RBBB > 10mm suggestive

37. Left Ventricular Hypertrophy
Compare these two 12-lead ECGs. What stands out as different with the second one?
The QRS complexes are very tall (increased voltage)
Normal
Left Ventricular Hypertrophy
Answer:

38. Boyd’s approach to LVH
** There are multiple systems advocated, at best 25 –50 % sensitivity. Meeting lots of criteria will increase sensitivity to nearly 95%.
Look at R in AVL; if >= 7.5 (some use 11mm), then + by Scott’s criteria.
I then pull my reference out and check other criteria; If questionable, state whose criteria you used.
If concerned, get an echo!!

39. LVH Dubin (Most specific, least sensitive) SV1 + RV6 >= 35
Robert’s (Most sensitive)
Total 12 lead QRS >175
Cassal’s
R aVl + S V3 > 28 m >20 w
Estes’
Scott’s
R in aVl > 7.5mm

41. Localizing Ischemia or Injury
aVF inferior
III inferior
V3 anterior
V6 lateral
aVL lateral
II inferior
V2 septal
V5 lateral
aVR
I lateral
V1 septal
V4 anterior

42. Anterior MI
Remember the anterior portion of the heart is best viewed using leads V1- V4.
Limb Leads
Augmented Leads
Precordial Leads

43. Lateral MI
So what leads do you think the lateral portion of the heart is best viewed?
Leads I, aVL, and V5- V6
Limb Leads
Augmented Leads
Precordial Leads

44. Inferior MI Leads II, III and aVF Limb Leads Augmented Leads
Now how about the inferior portion of the heart?
Limb Leads
Augmented Leads
Precordial Leads

45. Potassium summary:

46. Let’s look at some EKGs!!

47. Sample EKG #1. Determine rate, rhythm, diagnosis, axis

48. Interpretation EKG#1 Rate: approx 75/min
Rhythm: Baseline sinus rhythm, P:QRS is 1:1
Axis: Physiologic
Injury: ST elevation is present in the anterior, septal, and lateral leads. Massive ST segment elevation is present in V2-V6, with moderate ST elevation that obscures visualization of the QRS complex in lead one. Changes are consistent with LCA occlusion. Other: R wave progression is difficult to determine secondary to the pathological ST-T changes. No evidence of chamber enlargement or hypertrophy.

49. Sample EKG#2

50. Interpretation EKG#2
The EKG reveals an atrial flutter at a rate of approx 100 per minute. The QRS complexes are narrow and reveal a physiological axis. There is evidence of a premature ventricular complex, readily identifiable in the lateral chest leads. No evidence of ischemia or infarction. No evidence of R or L bundle branch block. Atrial flutter is conducted at approx 3:1. (3 flutter waves to one QRS).

51. Sample EKG#3

52. Interpretation EKG#3
The EKG reveals an irregularly irregular rhythm suggestive of atrial fibrillation. The rate is variable, with a controlled or slow ventricular response. The axis is physiologic. ST-T changes suggestive of ischemia/injury are present in leads II, III, and aVF. ST elevation of >1mm in limb leads is indicative of a possible inferior wall myocardial infarction. Reciprocal changes are seen in leads one and aVL. Early R wave progression.

53. EKG #4

54. Interpretation of EKG #4: This EKG reveals a baseline sinus rhythm
Interpretation of EKG #4: This EKG reveals a baseline sinus rhythm. Rate cannot be determined definitively. The QRS is wide; V1 reveals an RSR’ pattern consistent with a right bundle branch block. The axis is physiologic but is not easy to determine because of ST elevation present in leads III and aVF (inferior wall). Other abnormal T changes are seen (T wave inversion) in leads V1-V4. ST segment depression is present in the lateral chest leads as well. No evidence of chamber enlargement. ST elevation in III and aVF with reciprocal depression in I and aVL may be consistent with an inferior wall MI (RCA lesion.)

55. EKG #5

56. Interpretation of EKG#5: Baseline sinus rhythm
Interpretation of EKG#5: Baseline sinus rhythm. Rate appears normal (60-100) Axis is physiologic No evidence of block or conduction abnormality There is widespread ST segment elevation in all leads GLOBAL ST elevation is consistent with pericarditis

57. EKG #6

58. EKG #6 Interpretation: EKG #6 reveals a baseline sinus rhythm
EKG #6 Interpretation: EKG #6 reveals a baseline sinus rhythm. Rate approximately 80 bpm Axis is physiologic Complexes in V5 greater than 35 mm suggest LVH ST segment depression in leads V4-V6 in the setting of LVH is suggestive of a, “strain pattern”. No evidence of bundle brnach block ST segment depression in inferior chest leads

59. EKG #7

60. EKG #7 Interpretation:
Baseline sinus rhythm. Rate of approx 80/min Axis is physiologic No evidence of ventricular hypertrophy, but RAH is possible due to P wave in lead II >0.5 mm. Possible RBBB because of RSR’ in V1 and QRS >0.10 Note pathologic Q waves in II, III, aVF Pathologic Q waves are >0.04s or >1/3 the height of the R wave. Changes consistent with inferior wall myocardial infarction (old, possibly transmural). R wave progression preserved.

61. EKG #8

62. Interpretation of EKG #8:
Baseline sinus rhythm, rate approx 80. Right axis deviation, as evidenced by a primarily negative complex in lead I. Possible RAH due to large lead II P wave Possible RVH due to R>S in V1 Note pervasive strain pattern due to RVH evidenced in precordial leads. The presence of RAD plus the R>S in V1 is suggestive of RVH.

63. Any drug toxicity? EKG#8a

64. Digitalis effect summary: In addition to a wide variety of atrial conduction defects, ventricular ectopy, and heart blocks, early digitalis toxicity manifests itself as: a shortening of the QT interval in addition to scooped-out appearing ST segments.

65. EKG Interpretation #8a: Though the picture has poor resolution, it is clear that the lateral leads reveal a pattern of digoxin toxicity. Even though rate is impossible to determine, the “cored-out” and depressed ST segments in the lateral precordial leads suggest digoxin toxicity. Furthermore, the irregular R to R intervals hint at a baseline rhythm of atrial fibrillation. Many patients take digoxin for chronic atrial fibrillation. Moderate left axis deviation.

66. EKG #9

67. EKG #9: This rhythm strip reveals a profound bradycardia
EKG #9: This rhythm strip reveals a profound bradycardia. There is no relationship between the atria (P waves) and QRS complexes. This is consistent with complete A-V dissociation, or third degree heart block. This rhythm frequently requires emergent pacing.

68. EKG #10

69. EKG #10 Interpretation: This EKG reveals a baseline sinus rhythm (p’s are difficult to discern.) The rhythm is a sinus tachycardia at approximately 100 per minute. Massive ST segment elevation is present in leads II, III, and aVF. Reciprocal changes (depression) in leads I and aVL. Note that the precordial chest leads (v4R to V6R) are placed on the right side of the chest. ST segment in a “right-sided” EKG likely indicates an inferior wall MI that involves the RIGHT ventricle. Be careful when giving these patients NTG. Administration of nitrates, due to the alteration of venous preload, can precipitate hypotension. Treat these MI’s with fluid first. The axis is physiologic, no evidence of chamber enlargement. R wave progression is not of value in this EKG because of the right sided chest leads.

70. How about these rhythms?

71. Rhythm interpretation:
-The first strip reveals a prolonged PR interval, with 1:1 conduction. This rhythm is a first degree A/V block.
-The second strip is a 4:1 (or 3:1) atrial flutter.
-The third rhythm strip reveals the typical atrial fibrillation. Note the fibrillatory baseline with irregular R to R intervals.

72. End of part 4

73. Systematic approach R Roy RATE R Rogers RHYTHM I is INTERVALS A a AXIS
H horseback HYPERTROPHY
I icon INFARCT