1. FOCUS 1 ECG course
Dr. Boyd
SEMC

2. 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.

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

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

5. Acute Coronary Syndromes
Part 3:
Acute Coronary Syndromes

6. Case History
Mr. B. Skimmer, age 45, complains of chest “discomfort,” nausea, severe fatigue
Past Med Hx: hypertension (poor control), 2 to 3 pack/day cigarettes, high stress job
Refuses coworkers’ assistance
States: “It’s just the flu”
Goes to break room to rest

7. Should Mr. Skimmer go to ED by ALS ambulance? WHY?
Case Progression
One hour later a coworker finds Mr. Skimmer lethargic, pale, profusely diaphoretic
Coworker offers to drive Mr. Skimmer to ED, only 3 minutes away
Should Mr. Skimmer go to ED by ALS ambulance? WHY?

8. What should you — as the key ACLS provider — do first?
Case Progression
Mr. Skimmer arrives at your ED with O2 via NRB; IV KVO
Received “MONA” in field; BP dropped alarmingly, near syncope
Triaged as urgent
Placed in ED critical care bed
What should you — as the key
ACLS provider — do first?

9. The Five Quadrads Approach to ACLS-EP
1. Primary ABCD Survey
2. Secondary ABCD Survey
3. Oxygen–IV–monitor–fluids
4. Temp–BP–HR–RR
5. Tank–tank–pump–rate

10. Assessment Five Quadrads Approach
Primary Survey
Airway: adequate
Breathing: present with equal chest rise, adequate tidal volume
Circulation: pulse present carotid and radial
Defibrillation: not needed

11. Assessment Five Quadrads Approach
Secondary Survey
Airway: adequate
Breathing: lung sounds clear
Oxygen sat 97% with NRB
Circulation: sinus rhythm
2-mm ST-elevation in leads II, III, aVF
BP 126/84 mm Hg; IV access present
Differential diagnosis: AMI. Others?

12. Assessment Five Quadrads Approach
Oxygen–IV–monitor–fluids
Started by EMS; continued in ED
Vital signs
T=99.1°F, BP=126/84 mm Hg, HR=74 bpm, RR=28/min
Tank–tank–pump–rate
Consider sources of hemodynamic compromise

13. What would you like to do NOW?

14. Immediate ED Assessments
O2–IV–monitor–fluids (done by EMS)
Grade chest pain: character, intensity
H & P: focus on thrombolytic screening
VS — frequent recordings
Multilead ECG? (12, 15, or 22 leads)
First set serum markers
Electrolytes; coagulation studies
Portable chest film

15. 12-Lead ECG Findings 1. ST-segment elevation or new LBBB
strongly suspicious
for injury
2. ST-segment
depression/dynamic
T-wave inversion;
strongly suspicious
for ischemia
3. Nondiagnostic
or normal ECG;
chest pain strongly
suspicious for
ischemia

16. ECG 1: Interpretation?

17. ECG 1: elevated ST segments; inferior leads (II, III, aVF); ST depression: precordial leads V2-V5; lateral leads I, aVL Suspect occlusion — right coronary artery

18. 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

19. Coronary Artery Distribution
Left
Septal wall of LV
Anterior and lateral walls of LV
Inferior wall LV (10%)
Both bundle branches
Right
Inferior wall of LV (90%)
Posterior wall of LV
AV node (90%)
Right ventricle

20. Cardiac Anatomy in Relation to Coronary Artery
Right coronary artery
Septal wall V1-V2
Left anterior descending artery
Anterior wall
V3-V4
Left main coronary artery
Circumflex artery
Lateral wall I, aVL, V5-V6

21. Posterior View of the Heart
NOTE 1: Inferior wall supplied by either the right (85% to 90% of people) or left coronary artery.
NOTE 2: If there is acute injury in inferior leads (II, III, aVF), unknown whether left or right coronary artery is blocked.
NOTE 3: KEY — you must obtain a RIGHT-SIDED ECG at once.
Leads II, III, aVF
(from left coronary artery)
Lateral wall
Inferior wall
Right coronary artery
Posterior descending artery
Posterior wall
Circumflex artery
HOW TO GET RIGHT-SIDED ECG?

22. Lead Placement for a Right-sided ECGV1
V3R
V4R
V5R
V6R V2

23. Right Ventricular Infarction
Inferior lead changes  RV infarction?
Use lead V4R (ST elevation >1 mm)
Clinical significance:
Increased mortality
Preload dependence
Vasodilators may cause severe hypotension
What is management of RV infarction?

24. Coronary Insufficiency
Insufficient blood supply to the heart due to:
increased myocardial demand
decreased blood flow

25. Major Effects of Coronary Insufficiency
Ischemia
Injury
Infarct

26. ISCHEMIA Transient loss of myocyte function
Subendocardial layer most susceptible
Returns to normal rapidly with restoration of blood flow

27. INJURY Persisting myocyte damage with potential for recovery
Injured myocytes do not fully depolarize
Causes include
Non Q wave infarct
Prinzmetal’s variant angina

28. INFARCT Death of myocardial tissue
Infarcted tissue is electrically silent

30. J-point
J-point is the point at which the QRS complex meets the ST wave. ST segment elevation with an upward concavity is usually benign, especially when seen in healthy, asymptomatic individuals. ST segment elevation with a downward convexity is more likely to be due to acute coronary syndrome. Although ST elevation with an upward concavity and J-point notching often reflects a normal variant, this is only true if the patient is asymptomatic. The same ST pattern in a patient with chest pain is due to acute coronary syndrome until proven otherwise.

32. ISCHEMIA-EKG CHANGES ST straightening ST-T junction sharpening
Inverted U waves
ST segment depression (>1mm)
ST segment down-sloping
T wave inversion/symmetry

33. INJURY-EKG CHANGES Rapid ST elevation (>1mm)
Evolving T wave inversion

34. INFARCT- EKG CHANGES Tall peaked (hyperacute) T waves
ST elevation in area of infarct
Q waves in area of infarct
T wave inversion
Reciprocal changes

35. TIMELINE OF INFARCTION
Immediate Hyperacute T’s
Minutes ST elevation
Hours T wave depression
Days Q wave

36. HYPERACUTE T WAVES Immediately appear Greater than 5 mm limb leads
Greater than 10 mm precordial leads

37. Potassium summary:

38. ST ELEVATION Occurs within minutes Criteria for transmural injury:
> 1.0mm in two or more limb leads
> 2.0mm in two or more precordial leads

39. Q WAVES Duration more important than amplitude
Significance based upon:
clinical setting
width >.04 seconds
depth > 1/3 R wave
Septal Q waves are normal

40. ELEVATED ST SEGMENT
OTHER CAUSES

41. ST ELEVATION PNEUMONIC
Elevated ST,
think of “A PEA”

42. ELEVATED ST SEGMENT - PNEUMONIC
A cute MI
P ericarditis
E arly Repolarization
A neurysm

43. PERICARDITIS Early Diffuse concave upward ST elevation (Except AVR)
No Q waves or reciprocal ST changes
PR segments depressed in leads with upright P waves

44. PERICARDITIS Late
T waves invert -usually not until ST segments return to baseline !

45. PERICARDITIS
Can be focal:
surgery
trauma
acute MI

46. EARLY REPOLARIZATION Normal variant Upward concavity- Think fish hook!
J point begins with a notch or a slur

47. EARLY REPOLARIZATION No reciprocal ST changes
If ST elevation > 30% total T height,
early repol less likely

48. EARLY REPOLARIZATION CONTINUED
ST T WAVE
ST T WAVE

49. ANEURYSM ST elevation usually with deep Q wave or QS in same leads
ST - T wave changes are stable and persist for a long period

50. Other causes besides ischemia
DEPRESSED ST SEGMENT
Other causes besides ischemia

51. DEPRESSED ST SEGMENT Digitalis effect LV Strain Hypokalemia
Nonspecific ST changes
Resolving pericarditis

52. DIGITALIS EFFECT “Coved” ST depression especially lateral leads
Biphasic, flattened, inverted T waves
Decreased QTc interval

53. 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.

54. STRAIN PATTERNS Delayed repolarization of ventricle;
results in (-) ST and T wave segments
ST depression with upward convexity and T wave inversion

55. LVH with strain pattern
Edhouse, J. et al. BMJ 2002;324:
Copyright ©2002 BMJ Publishing Group Ltd.

56. STRAIN PATTERNS Lateral leads - THINK LVH
Anterior leads -THINK RVH or PE

57. STRAIN PATTERNS ST , T wave in leads with large R ST , T wave
in leads with large S

58. HYPOKALEMIA Prominent U waves Low voltage
Trough-like ST segment depression
T wave flattening, inversion or notching
QT interval prolongation
PR interval prolongation

59. NONSPECIFIC ST CHANGES
Changes that don’t fit criteria for ischemia infarct or strain
Most changes are normal variants

60. Diagnosing a MI
To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG.
12-Lead ECG
Rhythm Strip

61. The 12-Lead ECG
The 12-Lead ECG sees the heart from 12 different views.
Therefore, the 12-Lead ECG helps you see what is happening in different portions of the heart.
The rhythm strip is only 1 of these 12 views.

62. The 12-Leads The 12-leads include: 3 Limb leads (I, II, III)
3 Augmented leads (aVR, aVL, aVF)
6 Precordial leads (V1- V6)

63. Views of the Heart Lateral portion of the heart
Some leads get a good view of the:
Anterior portion of the heart
Inferior portion of the heart

64. ST Elevation
One way to diagnose an acute MI is to look for elevation of the ST segment.

65. ST Elevation (cont)
Elevation of the ST segment (greater than 2 small boxes) in 2 contiguous pre-cordial leads is consistent with a myocardial infarction (Greater than one small box in 2 limb leads)

66. Anterior View of the Heart
The anterior portion of the heart is best viewed using leads V1- V4.

67. Anterior Myocardial Infarction
If you see changes in leads V1 - V4 that are consistent with a myocardial infarction, you can conclude that it is an anterior wall myocardial infarction.

68. Putting it all Together
Do you think this person is having a myocardial infarction. If so, where?

69. Interpretation
Yes, this person is having an acute anterior wall myocardial infarction.

70. Other MI Locations
Now that you know where to look for an anterior wall myocardial infarction let’s look at how you would determine if the MI involves the lateral wall or the inferior wall of the heart.

71. Other MI Locations Lateral portion of the heart
Anterior portion of the heart
Lateral portion of the heart
Inferior portion of the heart
First, take a look again at this picture of the heart.

72. Other MI Locations Limb Leads Augmented Leads Precordial Leads
Second, remember that the 12-leads of the ECG look at different portions of the heart. The limb and augmented leads “see” electrical activity moving inferiorly (II, III and aVF), to the left (I, aVL) and to the right (aVR). Whereas, the precordial leads “see” electrical activity in the posterior to anterior direction.
Limb Leads
Augmented Leads
Precordial Leads

73. Other MI Locations
Now, using these 3 diagrams let’s figure where to look for a lateral wall and inferior wall MI.
Limb Leads
Augmented Leads
Precordial Leads

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

75. 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

76. 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

77. Putting it all Together
Now, where do you think this person is having a myocardial infarction?

78. Inferior Wall MI
This is an inferior MI. Note the ST elevation in leads II, III and aVF.

79. Putting it all Together
How about now?

80. Anterolateral MI
This person’s MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)!

81. ST Elevation and non-ST Elevation MIs

82. ST Elevation and non-ST Elevation MIs
When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time.
The ECG changes over time with each of these events…

83. ECG Changes Ways the ECG can change include: ST elevation & depression
Appearance of pathologic Q-waves
T-waves
peaked flattened inverted

84. ECG Changes & the Evolving MI
There are two distinct patterns of ECG change depending if the infarction is:
Non-ST Elevation
ST Elevation
ST Elevation (Transmural or Q-wave), or
Non-ST Elevation (Subendocardial or non-Q-wave)

85. ST Elevation Infarction
The ECG changes seen with a ST elevation infarction are:
Before injury
Normal ECG
Ischemia
ST depression, peaked T-waves, then T-wave inversion
Infarction
ST elevation & appearance of Q-waves
Fibrosis
ST segments and T-waves return to normal, but Q-waves persist

86. ST Elevation Infarction
Here’s a diagram depicting an evolving infarction:
A. Normal ECG prior to MI
B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves
C. Infarction from ongoing ischemia results in marked ST elevation
D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion
F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves

87. ST Elevation Infarction
Here’s an ECG of an inferior MI:
Look at the inferior leads (II, III, aVF).
Question: What ECG changes do you see?
ST elevation and Q-waves
Extra credit: What is the rhythm?
Atrial fibrillation (irregularly irregular with narrow QRS)!

88. Non-ST Elevation Infarction
Here’s an ECG of an inferior MI later in time:
Now what do you see in the inferior leads?
ST elevation, Q-waves and T-wave inversion

89. Non-ST Elevation Infarction
The ECG changes seen with a non-ST elevation infarction are:
Before injury
Normal ECG
Ischemia
ST depression & T-wave inversion
Infarction
ST depression & T-wave inversion
Fibrosis
ST returns to baseline, but T-wave inversion persists

90. Non-ST Elevation Infarction
Here’s an ECG of an evolving non-ST elevation MI:
Note the ST depression and T-wave inversion in leads V2-V6.
Question: What area of the heart is infarcting?
Anterolateral

91. Wellen’s warning
From this EKG you can predict what will be seen on Coronary Angiography So from the beginning, we have Sinus Rhythm, left atrial enlargement from the p morphology in V1, left axis deviation due secondarily to the Massive ACUTE ST ELEVATION MI localized by the ST Elevations in v2 through v5 which would be labeled "Antero-Lateral". But what is more important to notice on this EKG is the specific ST-Twave changes in v2-v3 which are labeled "Wellens Warning" or "Wellen's Sign" which represent Left Anterior Descending (LAD) artery stenosis/thrombosis.

92. In Figure 1 you can see the black arrows pointing to the specific ST-T wave findings that are labeled "Wellen's Warning" or "Wellen's Sign" which are present in our patients EKG.
This characteristic pattern was well reported in an article by Wellens and colleagues in 1962 in the American Heart Journal (Am Heart J 103:730, 1962) and was found to represent Critical Left Anterior Descending artery stenosis. Also found to represent impending stenosis if no ST-Elevations where present yet.
When examining patients for the first time with any type of unstable angina or chest pain symptoms with no ST changes but Wellen's warning present should not be taken lightly but aggressively pursued to rule out Ischemia.
Figure 2 is an example of a patient who presented with chest pain with no other EKG changes but these and went on to have a Massive MI due to a lesion of the LAD. So Even if there are no ST elevations this characteristic finding in v2 and v3 should not be over looked.
                            
                       

93. What do you see here?

94. Brugada syndrome

95. Brugada syndrome
Familial autosomal dominant (But majority of cases are sporadic)
St elevation V1 –V3, RBBB and T-wave inversion
Patients with this condition are at increased risk for sudden cardiac death, despite having structurally normal hearts

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

97. End of part 3