1. Essentials of 12-Lead ECG
Interpretation
HeartStart Skills Learning Center
826 Brookside Avenue, Suite A, Redlands, CA 92373
(909) 793-4555
www.heartstartskills.com
2. Topics
12-Lead ECG Overview
Critical Concepts of Acute Coronary Syndrome
Monitoring versus Diagnostic
Acquisition and Transmission
Axis Determination
Waveform Analysis
3. Topics
Injury, Ischemia or Infarction
Localization of Injury
Bundle Branch Blocks and Hemiblocks
ST Imposters
Differential Diagnosis of Wide Complex Tachycardias
4. What is the purpose of 12-Lead
ECGs?
• Demonstrated Advantages
– Rapid Identification of Infarction/Injury
• Diagnosis made sooner in many cases
– Decreased Time to Reperfusion Treatment
• Speeds preparation of & time to reperfusion therapies
– Increased Index of Suspicion
• Lowers false-negatives and false-positives
– Modification to Therapies
• From less invasive (Fibrinolytic) to aggressive (CABG) interventions
5. Critical Concepts in
ACS
• Ischemia
– lack of oxygenation
– ST segment depression or T wave inversion
• Injury
– prolonged ischemia
– ST segment elevation
• Infarct
– prolonged injury results in death of tissue
– may or may not show Q wave
6. Critical Concepts in ACS
ST elevation - the key to the acute reperfusion
therapy subset
You can’t see ST elevation without a 12-lead ECG
Perform on every patient suspected of ACS
Obtain early
Repeat frequently
10. Critical Concepts in ACS
Pain is Injury
Pain-Free is the Goal
Time is Muscle
Door to Reperfusion Therapy
“Time is the Tissue”
11. Monitoring vs Diagnostic
ECGs
Extra wires
3 wires versus 5 wires
• Monitoring Quality 12-Lead ECG
– Designed to provide information needed to determine
rate and underlying rhythm
– Designed to “filter out” artifact
• Reduces the amount and degree of electrical activity seen by
the ECG monitor
13. Monitoring vs. Diagnostic
ECGs
• Diagnostic Quality ECG
– Designed to accurately reproduce QRS, ST and T waveforms
– Designed to look more broadly at the cardiac electrical activity
– Unfortunately, may result in greater artifact being visible
15. Monitoring vs. Diagnostic
ECGs
Frequency Response
Term used to describe the breadth of the electrical spectrum
viewed by the ECG monitor
Diagnostic quality is usually 0.05 Hz to 150 Hz
Monitor quality is usually 0.5 Hz to 20-50 Hz
Usually printed on the ECG recording strip
21. Acquisition &
Transmission
Skin Preparation
Helps obtain a strong signal
When measured from skin, heart’s electrical signal about
0.0001 - 0.003 volts
Skin oils reduce adhesion of electrode and hinder
penetration of electrode gel
Dead, dried skin cells do not conduct well
22. Acquisition & Transmission
Other causes of artifact
Patient movement
Cable movement
- Electromagnetic Interference (EMI)
23. Acquisition &
Transmission
Patient Movement
Make patient as comfortable as possible
Supine preferred
Look for subtle movement
toe tapping, shivering
Look for muscle tension
hand grasping rail, head raised to “watch”
24. Acquisition & Transmission
Cable Movement
Enough “slack” in cables to avoid tugging on the
electrodes
Many cables have clip that can attach to patient’s clothes
or bed sheet
25. Acquisition & Transmission
• Electromagnetic Interference (EMI)
– Can interfere with electronic equipment
– 60 cycle interference is a type of EMI
– Look for nearby cell phones, radios or electrical devices
– No contact between cables & power cords
– Turn off or move away from AC devices
– Use shielded cables; inspect for cracks
30. Chest Lead Placement
V1: 4th ICS right of sternum
V2: 4th ICS left of sternum
V3: between leads V2 and V4
V4: 5th left midclavicular line
V5: level with V4 at left anterior
axillary line
V6: level with V5 at left midaxillary
line
32. ECG Accuracy
Look for:
Negative aVR
if aVR upright, look for reversed leads
One complete cardiac cycle in each lead
Diagnostic frequency response
Proper calibration
Appropriate speed
33. ECG Accuracy
Frequency Response
Display screen is non-diagnostic
Use the printed ECG for ST segment analysis
34. ECG Accuracy
Calibration
Voltage measured vertically
Each 1 mm box = 0.1 mV
1 mV = 10 mm
calibration standard
Confirm calibration
calibration impulse should be 10 mm (2 big boxes tall)
stated calibration should be “x 1.0”
36. ECG Accuracy
Paper Speed
Standard is 25 mm/sec
Faster paper speed means the rhythm will appear slower and
the QRS wider
Slower paper speed means the rhythm will appear faster and
the QRS narrower
39. When to
Acquire
Assessment Treatment
Vital Signs Oxygen
Oxygen Saturation Aspirin
IV Access Nitroglycerin
12-Lead ECG Morphine
Brief History
Modified from “The Ischemic Chest Pain Algorithm”, ACLS Textbook, American Heart Association, 2005.
40. Exposing the Chest
Immediately upon suspecting ACS...
Remove all clothing above the waist
Or, open shirt/blouse
Replace with gown (if possible)
Allows for complete exam
Minimizes wire entanglement
Enhances quick defibrillation if VF occurs
41. Essentials of 12 Lead
ECG Interpretation
Topics Discussed:
1. Anatomy Revisited
2. The 12 Lead ECG Device
3. The 12 Lead ECG Format
4. Waveform Components
5. Lead Views
42. Anatomy Revisited
RCA
Right Ventricle
Inferior wall of LV
Posterior wall of LV (75%)
SA Node (60%)
AV Node (>80%)
LCA
Septal wall of LV
Anterior wall of LV
Lateral wall of LV
Posterior wall of LV (10%)
43. Anatomy Revisited
SA node
Intra-atrial pathways
AV node
Bundle of His
Left and Right
bundle branches
left anterior fascicle
left posterior fascicle
Purkinje fibers
44. The 12 Lead ECG Device
Device serves as a voltmeter
Measures the flow of electricity
Unipolar versus Bipolar Leads
45. Bipolar Leads
• 1 (+) and 1 (-) electrode
– RA always (-)
– LL always (+)
– LA both (+) & (-)
• Traditional Limb Leads
are examples of these
– Lead I
– Lead II
– Lead III
• View from a vertical
plane
46. Unipolar Leads
1 positive electrode & 1
negative “reference point”
calculated by using summation
of 2 negative leads
Augmented Limb Leads
aVR, aVF, aVL
view from a vertical plane
Precordial or Chest Leads
V1-V6
view from a horizontal plane
48. The 12-Lead ECG Format
Device prints out 2.5 sec
each of Leads I, II, III then
switches to aVR, aVL, aVF
then switches to V1, V2,
V3 and then to V4, V5,
V6 (varies by device)
Device computer
analyzes all 10 sec of all
12 leads but only prints
2.5 sec of each group
49. The 12-Lead ECG Format
Not always
accurate
The computer IS
very accurate at
measuring
intervals &
durations
50. Waveform Components:
R Wave
First positive
deflection; R wave
includes the
downstroke returning
to the baseline
51. Waveform Components:
Q Wave
First negative
deflection before R
wave;
Q wave includes
the negative
downstroke &
return to baseline
52. Waveform Components:
S Wave
Negative deflection
following the R
wave; S wave
includes departure
from & return to
baseline
53. Waveform Components:
QRS
Q waves
Can occur normally in several leads
Normal Q waves called physiologic
Physiologic Q waves
< .04 sec (40ms)
Pathologic Q
>.04 sec (40 ms)
54. Waveform Components:
QRS
Q wave
Measure width
Pathologic if greater than or equal to 0.04 seconds (1 small box)
55. Waveform Components:
QS Complex
Entire complex is
negatively deflected; No R
wave present
56. Waveform Components:
J-Point
Junction between end of QRS
and beginning of ST segment;
Where QRS stops & makes a
sudden sharp change of
direction
76. Axis Determination & Deviation
Why Axis Determination?
The ability to identify hemiblocks (“fascicular blocks”) is the main
reason you need to be able to determine axis
77. Axis Determination & Deviation
“It is my opinion that the inability to determine the presence
of a hemiblock has often been the cause of complete heart
block when well-intentioned caregivers have improperly
administered Lidocaine.”
Mike Taigman, “Taigman’s Advanced Cardiology”, Brady, 1995, p. 71
78. Axis Determination & Deviation
What is Axis?
“the general (mean vector) direction of electrical impulses as they
travel through the heart”
“the sum total of all electrical currents generated by the ventricular
myocardium during depolarization”
normally from upper right to lower left
79. Axis Determination & Deviation
What do you need to determine the axis of an ECG?
The 12 Lead ECG
Leads CORRECTLY placed on the patient
RA on the right arm
LA on the left arm
LL on the left leg
Not on the chest or abdomen
Knowledge of axis deviation
80. Axis Reference
• Hexaxial Reference System
• The six frontal leads create
six poles that intersect at
the center of the heart
• Each pole has a positive &
negative axis
• Each + and - end is
assigned a value expressed
in degrees
• Hexaxial then divided into
quadrants (easier to use)
81. Axis Quadrants
Left axis -90°
-30 to -90 ° +120° -60°
aVL
Normal axis aVR
No LAD -30°
-30 to 90° -150°
Man’s
Land
Right axis +180° 0° I
90 to 180°
RAD Normal
+150° +30°
Extreme Right axis or
“No Man’s Land” +120° +60°
-90 to 180° III +90° II
aVF
82. Axis Determination
Quick Axis Determination
Determine the net QRS deflection in Leads I and aVF (positive or
negative)
Lead I aVF
Normal axis
LAD
RAD
ERAD
83. Axis Determination
Estimating Axis Quickly
Determine the net QRS deflection in leads I and aVF (-/+)
If the net QRS in Lead I is nearly the same as aVF, then axis midway
between or 45°
We estimate by calling it, “between +40° and +50°
If the net QRS in Lead I is positive and is obviously greater than aVF,
then axis closer to lead I
Estimate as “Between 0° and 40°”
If the net QRS in aVF is positive and greater than Lead I, then axis is
+50° and +90°
84. Axis Deviation
Pathologic versus Physiologic LAD
1. First step
a) Do I have LAD?
b) If yes, then proceed on
2. Look at Lead II
a) If the net QRS deflection is more negative than
positive, then the axis must be MORE NEGATIVE
than -30°
87. The Three I’s
Ischemia
lack of oxygenation
ST segment depression or T wave inversion
Injury
prolonged ischemia
ST segment elevation
Infarct
death of tissue
may or may not show a Q wave
88. Injury/Infarct Recognition
Well Perfused Myocardium
Epicardial Coronary Artery
Septum
Lateral Wall of LV
Positive Electrode
Interior Wall of LV
90. Injury/Infarct Recognition
Ischemia
Epicardial Coronary Artery
Septum Left Lateral Wall of LV
Ventricular
Cavity
Positive Electrode
Interior Wall of LV
91. Injury/Infarct Recognition
Ischemia
Inadequate oxygen to tissue
Represented by ST depression or T inversion
May or may not result in infarct or Q waves
95. Injury/Infarct Recognition
Injury
Prolonged ischemia
Represented by ST elevation
referred to as an “injury pattern”
Usually results in infarct
may or may not develop Q wave
114. Localization: Proximal RCA Occlusion
Right Ventricular Infarct (RVI)
12-lead ECG does not view right ventricle
Use additional leads
V3R - V6R
V4R
Right precordial leads
same anatomical landmarks as on left for V3 - V6 but placed on the right
side
116. Localization: ECG Evidence of RVI
Inferior MI (always suspect RVI)
Look for ST elevation in right-sided V leads (V3-V6)
117. Localization: Physical Evidence of RVI
Dyspnea with clear lungs
Jugular vein distension
Hypotension
Relative or absolute
118. Localization: Treatment for RVI
Use caution with vasodilators
Small incremental doses of MS
NTG by drip
Treat hypotension with fluid
One to two liters may be required
Large bore IV lines
119. Localization: Posterior Wall MI (PWMI)
Usually extension of an inferior or lateral MI
Posterior wall receives blood from RCA & LCA
Common with proximal RCA occlusions
Occurs with LCX occlusions
Identified by reciprocal changes in V1-V4
May also use Posterior leads to identify
V7: posterior axillary line level with V6
V8: mid-scapular line level with V6
V9: left para-vertebral level with V6
121. Localization: Left Coronary Dominance
Approximately 10% of population
LCX connects to posterior descending artery and dominates inferior wall
perfusion
In these cases when LCX is occluded, lateral and inferior walls infarct
Inferolateral MI
123. Localization Summary
Left Coronary Artery
Septal
Anterior
Lateral
Possibly Inferior
Right Coronary Artery
Inferior
Right Ventricular Infarct
Posterior
124. Evolution of AMI
• Hyperacute
– Early change suggestive of AMI
– Tall & Peaked
– May precede clinical symptoms
– Only seen in leads looking at
infarcting area
– Not used as a diagnostic finding
125. Evolution of AMI
Acute
ST segment elevation
Implies myocardial injury
occurring
Elevated ST segment presumed
acute rather than old
126. Evolution of AMI
• Acute
– ST segment Elevated
– Q wave at least 40 ms
wide = pathologic
– Q wave associated with
some cellular necrosis
127. Evolution of AMI
Age Undetermined
Wide (pathologic) Q wave
No ST segment elevation
Old or “age undetermined” MI
128. AMI Recognition
A normal 12-lead ECG DOES NOT
mean the patient is not having acute
ischemia, injury or infarction!!!
136. AMI Recognition
Reciprocal changes
Not necessary to presume infarction
Strong confirming evidence when present
Not all AMIs result in reciprocal changes
137. Summary
ST segment elevation is presumptive evidence for Acute
Myocardial Infarction
Other conditions may also cause ST elevation
Known as Imposters
141. Hemiblocks & Bundle Branch Blocks
Value
Help to identify patients at high risk for complete heart block
Hemiblocks, Bundle branch blocks and AV blocks are precursors to complete
heart block
You are Alert & Better Prepared!!!
142. Anatomy Review
Anatomy
Bundle of His
Left Bundle Branch
Anterior fascicle
long, thin; only blood supply from LAD
Posterior fascicle
shorter, thick; blood supply from RCA and LCX
Right Bundle Branch
143. Definitions
Hemiblock
Also called fascicular blocks
block in one of the two fascicles of the left bundle branch
Bundle Branch Block
block of the entire left or right bundle branch
144. Hemiblocks
Posterior fascicle
Much more difficult to have block greater disease
Less common but more concerning
Supplies majority of inferior wall of LV
If blocked, results in right axis deviation
145. Hemiblocks
Anterior fascicle
Easier to have block; More common
Supplies superior wall of LV
If blocked, results in pathologic left axis deviation
146. Hemiblock Identification
Left Anterior Hemiblock Left Posterior Hemiblock
Pathologic Left Axis Deviation Right Axis Deviation
small q wave in lead I small r wave in lead I
small r wave in lead III small q wave in lead III
Normal QRS or RBBB Normal QRS or RBBB
usually does have RBBB
“absence of right
ventricular hypertrophy
147. Precursors to Complete Heart Block
Any Type II AV Block
Anyone with disease of both bundles
Anyone with two or more of any blocks
Examples:
Prolonged P-R & anterior hemiblock
RBBB & anterior hemiblock
RBBB & posterior hemiblock
Prolonged P-R with anterior hemiblock & RBBB
148. Precursors to Complete Heart Block
If recognize precursors to CHB, then:
Have high index of suspicion for CHB
Have TCP ready (standby mode)
Patient may need a pacemaker
Administration of Lidocaine and other ventricular anti-Arhythmics
may result in CHB
Lidocaine contraindicated in patients with precursors to CHB unless TCP
in place and ready
149. Bundle Branch Block (BBB)
Can be pre-existing condition
Can be caused by ACS
If AMI caused
60-70% associated with pump
failure
40-60% mortality w/o reperfusion
150. Bundle Branch Block
Can Mimic or Hide Evidence Needed to Identify AMI
May Produce May Hide
ST elevation ST elevation
ST depression ST depression
Tall T waves Tall T waves
Inverted T waves Inverted T waves
Wide Q waves Wide Q waves
151. BBB Problem
BBB Problem
Critical to reperfuse patients with BBB produced by ACS
ACS “harder” to identify on ECG when BBB present
New or presumably new BBB is an indication for thrombolytic
therapy
155. Normal Ventricular Conduction
Normal Conduction
fibers of LBB begin conduction
impulse travels across interventricular
septum from left to right
towards + electrode creates small r wave
travels across ventricles causing
depolarization of both simultaneously
LV contributes most to complex
impulse travels away from + electrode
creates primarily negative complex
156. RBBB
RBBB in V1
no change in initial impulse
travel
small r wave
impulse depolarizes LV by
itself since RBBB
RV depolarized by impulse
thru muscle
it now contributes to
complex
travels toward + electrode
creating positive deflection
157. LBBB in V1
initial deflection altered LBBB
since travels right to left
now
Q wave or small q wave
RV depolarizes
unopposed
may produce small r
wave
travels across septum to
depolarize LV
deep S wave
159. BBB Recognition
• Use V1
• Find Terminal force
• Identify direction of terminal force
– Downward LBBB
– Upward RBBB
• Picture a Steering Wheel
– Right turn turn signal goes up
– Left turn turn signal goes down
163. Injury/Infarct Imposters
Some Common Examples (not all inclusive list)
Ventricular & Paced Rhythms
LBBB Conditions that make the identification of acute
injury/infarction DIFFICULT or IMPOSSIBLE
LVH
Benign Early Repolarization
Pericarditis
164. Injury/Infarct Imposters
Imposters can incorrectly place an ECG into any
of the three categories
ST Elevation ST Depression Normal
BBB T wave inversion Non-diagnostic
165. Ventricular & Paced Rhythms
Can mask or mimic every ECG change suggestive of
ischemia/injury
Paced rhythms
Idioventricular rhythms
V-Tach
PVCs
176. LVH Recognition
• Step 1
– Look in V1 and V2
– Pick the deepest negative deflection (S wave)
– Count small boxes of negative deflection in that lead
– Remember that number
178. LVH Recognition
• Step 2
– Look in V5 and V6
– Pick the tallest positive deflection (R wave)
– Count small boxes of positive deflection
– Remember that number
184. Benign Early Repolarization
Normal variant; Difficult to identify
Produces
ST elevation
Tall T waves
Changes usually seen in anterior & lateral leads
Most often seen in males ages 20-40
More common in African-American males
Thin, young persons
188. Pericarditis
May be viral, bacterial or metabolic
Secondary to recent cardiac surgery
Post MI
IV Drug abuse
Clinical presentation may include CP
Often produces diffuse ST elevation on ECG plus clinical
presentation
189. Pericarditis
Correlate Diffuse ST segment elevation with Clinical Presentation
Sharp, “Stabbing” chest pain
Can be localized
May be relieved by movement, respiration, position, swallowing
May radiate to base of neck, between shoulder blades
190. Pericarditis
May produce ST elevation in any lead
May be in all leads
May not be anatomically grouped
J-point notching often present
Fish hook
192. Summary
Imitators can produce ST elevation or depression
Imitators can eliminate ST elevation or depression
Most frequent imitators
LVH
BBB
Paced rhythms
193. Summary
Imitators can produce ST elevation or depression
Imitators can eliminate ST elevation or depression
Most frequent imitators
LVH
BBB
Paced rhythms
194. Summary
• If QRS is wide
– Consider BBB
– Consider ventricular rhythm (or paced)
• If QRS is narrow
– Consider LVH
– Consider pericarditis
– Consider early repolarization
195. Summary
“Fish hooks” often seen with:
Pericarditis
BER
“Fish hooks” can also be seen with ACS
196. Summary
The presence of a potential imposter
DOES NOT ALWAYS
make it impossible to identify injury/infarction
Editor's Notes
This information will aid in understanding the ECG subsets in the next section. Define ischemia, injury and infarct. Note that the definitions are correlated with specific ECG criteria. Note that “injury” is also ischemia and does not imply any permanent damage or death to tissue. The term injury simply means ischemia identified by ST segment elevation.
While it is not always possible to identify which of the ACS a patient is experiencing, it is possible to determine if a patient can benefit from acute reperfusion therapy. The indication for acute reperfusion therapy is ST segment on the 12-lead ECG. For EMS to identify this subset of patients, a diagnostic 12-lead must be obtained . “ The 12-lead ECG stands at the center of the decision making pathway in the management of patients with ischemic chest pain, and delays in obtaining the 12-lead ECG must be eliminated.” AHA, ACLS Textbook, 1997, 9-13
Whether tissue necrosis occurs as in AMI or does not occur resulting in unstable angina is determined by the interplay of several factors. This underscores why it is usually impossible to determine which syndrome is present and why we should instead concentrate on identifying the the presence of any ACS. The issue of suspecting ACS will be addressed after a brief explanation of the terms ischemia, injury and infarction.
Thrombolytics are pharmacological agents administered IV that dissolve a coronary thrombus. PTCA is an intervention that utilizes a balloon or other device, inserted through a large artery, to create a larger lumen in the offending coronary artery. Atherectomy procedures remove the occlusion by laser or cutting mechanisims.
The typical “3-lead” ECG was never designed to capture QRS-ST-T waveforms with complete accuracy. The 3-lead was designed to provide enough information for the user to determine cardiac rate and rhythm. Because artifact makes interpretation difficult, the 3-lead is set to “filter out” artifact by reducing the spectrum of cardiac electrical activity that it “sees”. This strategy significantly reduces artifact and still renders waveforms of sufficient quality for rate and rhythm determination. However, in doing so, the QRS-ST-T may not always be accurately represented. Therefore, do not use monitor quality for ST analysis.
The 12-lead is designed to accurately reproduce the QRS-ST-T waveforms. In order to do so the 12-lead must “look” at a broader spectrum of cardiac electrical activity. This spectrum is referred to as “frequency response” This broader spectrum is referred to as “diagnostic quality”. A diagnostic quality ECG is necessary for accurate ST segment analysis. Unfortunately, when in diagnostic quality, all 12-lead ECGs are more susceptible to more artifact than are 3-lead ECGs.
The frequency response is printed on the ECG paper. The frequency response for diagnostic quality is 0.05Hz - 150Hz. There may be some slight variation among manufacturers and ECG models. The low end for monitor quality is often 0.5 Hz (not 0.05Hz), while the high end often is in the range of 20-50Hz.
The frequency response is printed on the ECG paper. The frequency response for diagnostic quality is 0.05Hz - 150Hz. There may be some slight variation among manufacturers and ECG models. The low end for monitor quality is often 0.5 Hz (not 0.05Hz), while the high end often is in the range of 20-50Hz.
Because of the increased “window” to electrical signals, additional steps must be taken to reduce the amount of artifact produced. Removing excess hair and prepping the skin allows the electrode gel to better penetrate the skin, thus receiving a stronger signal with less artifact. First we will discuss the techniques themselves, later in the module we will look at strategies to accomplish these additional tasks quickly.
Excess hair presents two problems: • First, hair may prevent the electrode from adhering well. • Second, hair may inhibit gel contact and skin penetration. Some thrombolytic manufacturers recommend that clippers be used to remove chest hair. The intent is to minimize the potential for bleed sites in a patient who may receive a thrombolytic.
Simply rubbing the skin with a gauze pad can have a noticeable effect on ECG clarity by: • Reducing skin oil • Removing part of the stratum corneum
When measured from the patient ’s skin, the heart’s electrical signal is extremely small, about 0.0001 to 0.003 volts. That ’s as small as one-ten thousandth of a volt. Compare this with energy from a nine volt battery. Good skin prep will make the ECG signal as strong as possible, and make the artifact signals as small as possible.
Once the skin has been prepped and the electrodes applied, there are still other sources of artifact to consider.
It is important to place the patient in a position of comfort. The reduction in muscle tension will help to prevent artifact. When possible, the patient should be in the supine position for a 12-lead ECG. Sometimes this is not feasible, practical or desirable. If ECG is not recording in supine position, simply note this on ECG.
It is important to place the patient in a position of comfort. The reduction in muscle tension will help to prevent artifact. When possible, the patient should be in the supine position for a 12-lead ECG. Sometimes this is not feasible, practical or desirable. If ECG is not recording in supine position, simply note this on ECG.
It is important to place the patient in a position of comfort. The reduction in muscle tension will help to prevent artifact. When possible, the patient should be in the supine position for a 12-lead ECG. Sometimes this is not feasible, practical or desirable. If ECG is not recording in supine position, simply note this on ECG.
Note how the baseline straightened out by simply repositioning the patient cables and clipping them onto the sheet. What technique(s) would you consider in order to resolve the muscle artifact?
All of the techniques discussed to this point have related to ECG clarity. We now need to look at what is necessary to ensure ECG accuracy.
Limb leads should be placed on the limbs. The traditional placement is near the ankles and wrists.
V1 fourth intercostal space to the right of the sternum V2 fourth intercostal space to the left of the sternum V3 directly between leads V2 and V4 V4 fifth intercostal space at left midclavicular line V5 level with lead V4 at left anterior axillary line V6 level with lead V5 at left midaxillary line
Here is what lead placement looks like on a patient.
Once a clear ECG has been obtained (free of excess artifact and has a steady baseline), it may then quickly be examined to confirm accuracy. Listed here are five items that relate the the accuracy of the ECG.
It is important to note that the display screen in 12-lead monitors is not in diagnostic quality. Usually a 12-lead must be printed out for accurate ST analysis. Check the 12-lead printout and confirm the correct frequency response.
It is important to note that the display screen in 12-lead monitors is not in diagnostic quality. Usually a 12-lead must be printed out for accurate ST analysis. Check the 12-lead printout and confirm the correct frequency response.
It is important to note that the display screen in 12-lead monitors is not in diagnostic quality. Usually a 12-lead must be printed out for accurate ST analysis. Check the 12-lead printout and confirm the correct frequency response.
These tracings show how much the ECG can change in a short time. Note the times on these ECGs.
This excerpt from an American Heart Association algorithm shows the initial 12-lead acquisition along with the vital signs. Note treatment is concomitant and is not inordinately delayed. In later modules we will further develop the concepts relating to the dynamic nature of AMI and the 12-lead ECG. At that time it will be very apparent why early ECGs are critical. Accepting that fact necessitates a strategy for QUICK 12-lead acquisition
Exposing the chest before obtaining the 12-lead is probably the single most important factor to reduce time and effort. If a gown is not available a sheet may be used, however, the gown is preferable.
ST segments are iso-electric.
Define ischemia
Note widespread ST depression and T waves inverted in several leads.
Define injury. Ischemia affecting the epicardium represented by ST elevation.
Ask group to look for ST elevation.
Death of tissue.
Pathologic Q waves present in II, III and aVF suggest necrosis has occurred in the inferior region of the left ventricle.
A normal ECG does NOT rule out any Acute Coronary Syndrome.
EXERCISE: approximately 2 minutes 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 checkmark next to any lead with 1mm of ST segment elevation. Review findings with group, pointing out every J-point and ST segment. Note leads II, III and aVF display elevation. Remember ST segment elevation is presumptive evidence for AMI. Knowing which part of the heart leads II, III and aVF “sees” would tell you where the infarct is located.
This represents the 3x4 format of the 12-lead ECG. Each box represents one lead, and the viewpoint of that lead is indicated.
Each box represents one lead, and the viewpoint of that lead is indicated. NOTE: Refer participants to their pocket card where this information is summarized as well.
The three subdivisions of the LCA.
Note the change and locate the anatomical territory affected, correlate to the suspected coronary artery. This involves the septal and anterior leads. Commonly called antero-septal MI.
Note the change and locate the anatomical territory effected, correlate to the suspected coronary artery. This involves the lateral leads. Called lateral wall infarct.
Note the change and locate the anatomical territory effected, correlate to the suspected coronary artery. This involves septal, anterior and lateral leads. Commonly referred to as extensive anterior.
When the proximal LCA (a.k.a. left main) is occluded, the entire left coronary territory is effected. This includes the septal, anterior and lateral walls; this is referred to as an acute extensive anterior MI. Complications such as LVF with pulmonary edema and/or cardiogenic shock are common and expected. Mortality is high.
Thrombolytics work well for extensive anterior MI ’s when the BP is elevated or normal. When cardiogenic shock is evident, a trip to a surgical capable cath lab is indicated because these lesions often require emergency bypass surgery.
The bundle branches are primarily supplied by the LCA.
The right coronary artery includes the proximal RCA and the PDA.
This ECG 4 is an IWMI. The RCA is occluded somewhere along its course. From this view you cannot conclude if the lesion is proximal or distal.
If the lesion is proximal (high in the RCA), then right ventricular infarct may result. Additional leads are needed to see the right ventricle.
Note obvious acute IWMI. The right chest leads (V4R, V5R and V6R) show ST elevation including RVI. The proximal RCA must be occluded .
Evidence of acute IWMI is an indication to examine the right precordial leads.
These signs are due to failure of the right ventricle during an acute RVI.
If normotensive, supinate patient if possible, have fluid line established, consider small (200cc) fluid challenge, then administer NTG via drip and small incremental doses of MS for pain. NTG via spray or tab can be used if drip not available, be ready for hypotension. If hypertensive, significant failure from RVI is unlikely.
Posterior wall MI ’s rarely occur alone, they are usually an extension of a lateral or inferior MI. The posterior wall has a dual blood supply. It receives blood from the RCA and LCA.
Note acute posterior wall MI.
In these cases, when the LCX occludes, the lateral and inferior walls infarct.
Note infero-lateral MI.
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.
ST segment elevation is the next probable ECG change. ST segment elevation implies at least three things: 1. Myocardial tissue injury is presently occurring. 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.
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.
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.
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.
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. Antero-septal
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)
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. Lets talk about one cause of ST depression, known as reciprocal ST depression.
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.
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.
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.
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
Not all AMIs with ST elevation produce reciprocal depression. Quite simply… some do and some don ’t. When reciprocal depression is noted, the likelihood of AMI is dramatically increased.
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.
Bundle Branch Block (BBB) has a number of potential causes. BBB can be the result of a fibrosis or calcification of the ventricular conduction system. (Lev ’s disease and Lenegre’s disease are examples.) People can live well for many years with the BBB caused by these conditions. Unless there is evidence of worsening conduction (syncope, dropped beats, etc) these conditions are non-emergent. BBB can also be caused by an ACS. When BBB is caused by an ACS, it identifies a very high risk patient!
Literally, BBB can both mask and mimic all of the ECG changes associated with ACS!
The presence of a new BBB, or presumably new BBB, is an indication for thrombolytic therapy*. At the physician ’s discretion, thrombolytics may be administered to patients whose BBB obscures the diagnosis of AMI on the ECG. *The 1996 ACC/AHA Guidelines for the Management of Patients with Acute Myocardial Infarction ” lists BBB as a Class I indication for thrombolysis. (Definition of Class 1: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is beneficial, useful, and effective)
BBB widens the QRS (120ms or more). This widening is due to the fact that the ventricles are forced to contract sequentially, thus requiring more time. Other conditions widen the QRS; a common one would be ventricular rhythms either paced or spontaneous. A differentiating factor between BBB and ventricular rhythms would be the presence of an underlying supraventricular rhythm. Therefore, when a QRS of 120ms or more is produced by a supraventricular rhythm, think BBB. This rule applies in all leads.
Example 1 underlying rhythm sinus QRS width 160ms Example 2 underlying rhythm sinus QRS width 120ms
Example 1 underlying rhythm sinus QRS width 160ms Example 2 underlying rhythm sinus QRS width 120ms
The “classic” pattern for RBBB in V1 is an RSR.
The “classic” pattern of LBBB in V1 is a QS complex. There are many variations to these classic patterns, complicating the process of distinguishing RBBB from LBBB. In addition, each form of BBB produces a different set of changes in V6. Fortunately, a simplified approach does exist.
After BBB has been determined to exist, look at lead V1. To identify the terminal force, first locate the J-point. From the J-point, back up about 40 ms into the QRS. Now determine if the terminal force (tail end) is pointing up or down.
Always remember, the following rules for differentiating RBBB from LBBB apply only to V1. We will learn to identify the terminal force of the QRS in V1, and determine if it is positive or negative. Simply stated, we will look at the tail end of the QRS complex and decide if it points up or down.
Have the participants review these four examples of V1 in the course guide and determine if the BBB is LBBB or RBBB.
Any rhythm or beat originating in the ventricles can imitate the ECG changes associated with ACS. NOTE: Sometimes caregivers are less likely to make the interpretation of a ventricular rhythm when the heart rate is greater than 60 but less than 150. Ventricular rhythms can and do occur at this “in between” rate and are referred to as accelerated idoventricular rhythms (AIVR).
Here is an example of how ventricular rhythms can imitate changes suggestive of ACS. Remember, they can mask the changes as well.
There are many causes of LVH. Most are the result of either the left ventricle working harder over a long period of time or the result of chronic overfilling. For ACS management, it is NOT critical to determine the cause of the LVH. Simply suspecting the presence of LVH is sufficient.
LVH can both mask and mimic all of the ECG changes associated with ACS!
Unlike BBB and ventricular rhythms, LVH does NOT usually widen the QRS to 120ms or more. Instead of abnormally widening the QRS, LVH increases its amplitude. There are many formulas for suspecting the presence of LVH. The three step method described here is one of the simpler means of suspecting LVH. Remember, we are not trying to identify LVH for its own sake. Rather we seek to identify LVH as a potential imitator of ACS.
Participants review this tracing in their course guide while instructor describes method of LVH recognition.
STEP 1 Compare V1 and V2. Determine which is the deepest negative deflection. In the deepest lead, count the millimeters of negative deflection.
Hypertrophy often causes overlapping of ECG leads which may make counting boxes in V1 and V2 difficult.
STEP 2 Compare V5 and V6. Determine which is the tallest. In the tallest lead, count the millimeters of positive deflection.
STEP 3 Add the two numbers together. If their sum equals 35 or more, suspect LVH is present.
Look again at the ECG, look to see which leads show changes suggestive of LVH. (Point out ST elevations, depressions, T wave inversions.) Could all of these changes be due to ACS? (yes) Could all of these changes be due to LVH? (yes) How would you manage such a patient? If the story suggests ACS, that is how the patient is managed.
Despite the obvious ECG changes seen here, this ECG was obtained from a patient with a perfectly normal heart! It is an example of a normal variant called “Benign Early Repolarization”.
It has been theorized that the cause of BER is due to one region of myocardium repolarizing early. This produces a difference in electrical potential, and thus causes ST and T wave changes.
One ECG sign that should make you consider BER is the notched J-point, creating a fish hook like appearance of the ST segment.
A notch at the J-point is shown here. NOTE: The presence of “fish hooks” does not rule out ACS. It is not uncommon to see J-point notching as a result of ACS. NOTE: Patients with BER often meet the voltage criteria for LVH. However, no true hypertrophy may exist.
This ECG has ST elevations and some similarities to BER. However, in this case, BER is not present. This is an example of pericarditis.
There are numerous causes of pericarditis. These patients often complain of chest pain, which is an indication for a 12-lead. Pericarditis is capable of producing ST changes on the ECG.
The “classic” pericarditis presentation has some distinguishing features. The purpose of the following description is not to rule out AMI, but to help the care provider suspect the possibility of pericarditis. Classic presentation: • Sharp chest pain (meaning a stabbing nature, not meaning intense) • Pain can often be localized with one finger • Pain may radiate to the base of the neck or between the shoulder blades (trapezius area)
The ST elevation of pericarditis is caused by inflammation of the epicardium secondary to inflammation of the pericardium. This process is not related to coronary artery disease and, therefore, ST changes do not tend to follow anatomical groups typically seen with ACS. Like BER, pericarditis may produce a notching of the J-point and a “fish hook” shaped ST and J-point.
Certainly medications have the potential to affect the ECG. One of the best documented changes due to a medication is the digitalis effect.
Correct categorization of ECG changes can be complicated when an imitator is present. These imitators can lead to erroneous placement of a patient into the ST elevation or ST depression category. The imitators can also mask changes that would have otherwise been present on the ECG.
Correct categorization of ECG changes can be complicated when an imitator is present. These imitators can lead to erroneous placement of a patient into the ST elevation or ST depression category. The imitators can also mask changes that would have otherwise been present on the ECG.