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STEMI Training
1. 12 Lead EKG Interpretation
and STEMI Management
2. Who Are These Clowns?
Michael Grzyb
NREMT - Paramedic
17 years EMS Education Experience
ACLS, PALS, BCLS, BTLS Instructor
EMS Management – Clinical Services,
Education and Training, and CQI
ZOLL Medical
Senior Manager, EMS Clinical Deployment
3. Who Are These Clowns?
Jeffrey Rupple
NREMT – Paramedic
20 years EMS Education Experience
PALS, BCLS Instructor
EMS Management – Director of Operations,
Field Supervisor, Field Training Officer
ZOLL Medical – Clinical Deployment Specialist
4. Disclaimer
Information contained herein is provided
for reference only and does not replace
local / regional standing orders,
protocols, Standard Operating
Procedures or equipment manufacturer’s
recommendations.
5. Disclaimer
The information and tools presented to you today are
outstanding aids to your patient assessment and
treatment, and ideally will enable you
to provide better patient care.
The devices and information provided are designed to
AUGMENT your patient assessment
NOT REPLACE IT!
PLEASE,
TREAT THE PATIENT, NOT THE MONITOR!
6. Benefits of Prehospital 12-Lead ECG
Recognize AMI
Identify Reperfusion Candidates
The Earlier the Better - TIME IS MUSCLE!
Reduce Time to Thrombolysis
Reduce Time to PCI
Prehospital Thrombolytics
8. Myocardial Infarction Labels
For pre-hospital purposes
Non- ST- Elevation MI (NSTEMI) = Non-Q-Wave MI
(NQMI)
ST Elevation MI (STEMI) = Q-Wave MI (QMI)
11. ACS Risk Factors
Diabetes
Smoking
Hypertension
High Cholesterol
Family History
Obesity
Sedentary Life
12. The History
Good Assessment
• HPI
• Nature of Symptoms
• OPQRST
• Patient History
Traditional Risk Factors
• Age
• Male Sex
• DM
• Tobacco
• History of CAD
• Family History
• HTN
• Cholesterol
Non-Traditional
Risk Factors
• DM = CAD
• HIV with or without
HAART
• Cocaine/Meth
• CRI
• SLE
14. Chest Pain
Anginal (Ischemic) - Fullness, pressure,
crushing may radiate to neck, jaw, back, etc.
Atypical - Unilateral, sharp, changes with
position, pleuritic, muscular-skeletal, not in
chest but in jaw, neck, back
16. Misdiagnosis
Misdiagnosed Chest Pain is the single largest area of
litigation against Emergency Room Physicians. MACEP 2005
Patients with ACS may have chest wall tenderness on
palpation. MACEP2005
One survey included 600,000 patients diagnosed with
M.I. Study included 25% of all hospitals in US. One
question asked…
Did you have chest pain at any point?
33% of all patients survey answered “NO”
17. Misdiagnosis
Although traditionally deemed as low risk:
• Pleuritic
• Sharp and stabbing pain,
• Pain reproducible with palpation or movement
• Pain that is either very short or prolonged in
duration
A significant number of patients diagnosed with M.I.
presented with these symptoms*
One study revealed that 7% of all M.I. patients
evaluated had pain that was fully reproducible on
palpation*
*Lee TH, Cook EF, Weisberg M, et al Acute chest pain in the ED, Arch
Internal Med.
18. MONA for all ACS patients?
Morphine
Oxygen?
NTG
ASA
12 Lead EKG
Transport Dx!
Beta Blockers?
19. Therapy: What does it get me?
Aspirin
• 21-25% reduction if given during ACS and continued
out 35 days (ISIS-2, JACC 1988)
Beta-blocker
• Clearly shown to reduce all-cause mortality long term
following ACS
• Possible 1% reduction in re-infarction and VF is offset
by the 1.1% of patients who end up in cardiogenic
shock when it is inappropriately given
(COMMIT/CCS-2, 2005)
21. Relationship Between DBT and Mortality
Deluca G et al. Time delay to treatment and mortality in primary angioplasty for AMI: every
minute of delay counts. Circulation 2004; 109(10): 1223-1225
30 minute delay
= 7.5% increase
in mortality!
22. Value of an Early ECG
ECG changes from ACS are dynamic
MONA treatment may mask changes
ST elevation = reperfusion indication
EMS is in a privileged position
• Early 12-lead
• During symptoms
• Before medication
23. Reduce Time to Thrombolysis
Many studies have shown significant
reductions in hospital-based time to
treatment with fibrinolytic therapy in
patients with AMI identified before arrival
by 12-lead ECG. Time savings ranged from
20-55 minutes.
AHA, Guidelines 2000
24. Bradley EH, et al. N Engl J Med. 2006. November 13. [Epub ahead of print].
Strategies Associated With a Significant
Reduction in Door-to-Balloon Time
Strategy
Mean reduction in
door-to-balloon
time (min)*
Having emergency physicians activate the cath lab 8.2
Having single call to a central page operator activate cath lab 13.8
Having the ED activate the cath lab while patient still en route 15.4
Expecting staff to arrive at cath lab within 20 minutes after
page
19.3
Having an attending cardiologist always on site 14.6
Having staff in ED and cath lab use and receive real-time
feedback
8.6
25. Who Are These Clowns?
Jeffrey Rupple
NREMT – Paramedic
20 years EMS Education Experience
PALS, BCLS Instructor
EMS Management – Director of Operations,
Field Supervisor, Field Training Officer
ZOLL Medical – Clinical Deployment Specialist
26. Who Are These Clowns?
Jeffrey Rupple
NREMT – Paramedic
20 years EMS Education Experience
PALS, BCLS Instructor
EMS Management – Director of Operations,
Field Supervisor, Field Training Officer
ZOLL Medical – Clinical Deployment Specialist
28. Obtaining the 12-Lead ECG
Remove the patient’s clothes from waist up
• Prevents wire tangle
• Permits full chest exam
• Allows for rapid defibrillation if needed
• Saves time in ER
• Use a hospital-type gown
Real World - adjust clothing as appropriate for
surroundings
29. Obtaining the 12-Lead ECG
Clip chest hair
• Faster
• More comfortable
• Prevents infection
• Safer (less nicks and cuts)
Shaving is acceptable alternative
• Think gross decon
• Not Remington close
30.
31. Obtaining the 12-Lead ECG
Prep the skin
• Should be done prior to EVERY 12-Lead ECG
• 12 Lead is more sensitive to artifact
• Use commercially prepared skin preps if available
• 4x4 gauze pads or towel with firm, brisk rub works
well
• Cardiac Services (Cath Lab, EP Lab) use fine grit
sandpaper!
• DON’T BE TIMID!
32.
33. Obtaining the 12-Lead ECG
Position patient correctly
Supine is ideal
Recline patient as low as they will tolerate
Below 45 degrees is acceptable
Have patient remain still
Watch for muscle tensing (White Knuckle)
Indicate symptoms, treatment, and time
34.
35. Causes of Poor Tracings
Causes of poor ECG signal
• Most common cause is poor electrode contact with
skin
Check for
• Excessive hair
• Loose or dislodged electrodes, especially in
diaphoretic (sweaty) patients
• Dried conductive gel on disposable electrodes
• Poor placement over bony area
• Poor quality electrodes
36. Disclaimer
Information contained herein is provided
for reference only and does not replace
local / regional standing orders,
protocols, Standard Operating
Procedures or equipment manufacturer’s
recommendations.
37. Electrode Quality
ZOLL recommends the use of a high quality
wet gel electrode
Dry gel electrodes do not perform well in the
EMS environment
Poor quality electrodes are more likely to
provide poor quality tracings
40. Lead Placement
V1 - Right parasternally, 4th ICS
V2 - Left parasternally, 4th ICS
V3 - Between V2 and V4
V4 - 5th ICS, mid clavicular line
V5 - Between V4 and V6
V6 - Left mid-axillary line, (level with V4)
41. Indicative Leads
Positive Pole (+)
Acts as point of reference
Imagine the positive pole as a camera lens
42.
43. 4 Lead Placement for 12 Lead ECG
Contrary to popular belief, the 4 primary
monitor leads, often referred to as limb leads,
DO NOT need to be placed on the distal
extremity (i.e. wrists and ankles)
The primary leads need to be 10 centimeters
(approximately 4 inches) from the heart to be
diagnostically significant (accurate)
Distal lead placement originates from Dr.
Willem Einthoven original EKG experiments in
the early 1900s
45. Distal Lead Placement
If you are still using the machine from the
previous slide, then yes, distal lead placement
is required
46.
47.
48.
49.
50. Indicative Lead Groups
Inferior Wall - II, III, and aVF
Septal Wall - V1, V2
Anterior Wall - V3, V4
Lateral Wall - V5, V6, I, and aVL
51. Disclaimer
The information and tools presented to you today are
outstanding aids to your patient assessment and
treatment, and ideally will enable you
to provide better patient care.
The devices and information provided are designed to
AUGMENT your patient assessment
NOT REPLACE IT!
PLEASE,
TREAT THE PATIENT, NOT THE MONITOR!
52. Disclaimer
The information and tools presented to you today are
outstanding aids to your patient assessment and
treatment, and ideally will enable you
to provide better patient care.
The devices and information provided are designed to
AUGMENT your patient assessment
NOT REPLACE IT!
PLEASE,
TREAT THE PATIENT, NOT THE MONITOR!
53. Disclaimer
The information and tools presented to you today are
outstanding aids to your patient assessment and
treatment, and ideally will enable you
to provide better patient care.
The devices and information provided are designed to
AUGMENT your patient assessment
NOT REPLACE IT!
PLEASE,
TREAT THE PATIENT, NOT THE MONITOR!
54.
55. Presumptive Evidence of an AMI
Presumptive evidence of an AMI
• One mm of ST elevation in 2 leads from any group
• 2 contiguous chest leads
Contiguous Leads- Anatomic or Numerical
New or “presumably new” Left BBB?
The standard 12-Lead does not have leads
facing the posterior left ventricle or the right
ventricle. Specialty leads are required to detect
these type of MI’s.
58. Survey Says
ST elevation in the inferior leads
II, III and aVF
Acute inferior myocardial infarction
59.
60. Oh Boy!
ST elevation in the septal, anterior and lateral
leads
V1 - V6, I and aVL
Acute anterior-lateral myocardial infarction
61. Benefits of Prehospital 12-Lead ECG
Recognize AMI
Identify Reperfusion Candidates
The Earlier the Better - TIME IS MUSCLE!
Reduce Time to Thrombolysis
Reduce Time to PCI
Prehospital Thrombolytics
62. Benefits of Prehospital 12-Lead ECG
Recognize AMI
Identify Reperfusion Candidates
The Earlier the Better - TIME IS MUSCLE!
Reduce Time to Thrombolysis
Reduce Time to PCI
Prehospital Thrombolytics
65. Right Coronary Artery
Supplies the inferior wall of
the left ventricle and feeds
the right ventricle
Branches off into the
posterior descending
coronary artery which…
Supplies the posterior wall
of the left ventricle.
Inferior wall MIs have
posterior and/or right
ventricular involvement in
50% of the cases.
66. Left Anterior Descending
The left anterior descending (LAD) coronary
artery is a major branch of the LCA
LAD feeds 40% of the left ventricular mass
Because most sudden-death AMI’s result from
a proximal occlusion of the LAD, it is known as
the “Widow Maker”
LAD feeds the anterior and septal walls of the
left ventricle
LAD also supplies the Bundle of His and both
branches through the intraventricular septal
perforator artery
67. Adding Insult to Injury
40% involvement of
the left ventricle
results in irritation
that can cause
immediate v-fib or v-
tach
Patients may develop
CHB, BBB’s or
hemiblock as another
complication of LAD
proximal occlusion
68. Left Circumflex Artery
Is the other major
division of the left
coronary artery
The LCA feeds the
lateral and posterior
walls of the left
ventricle
73. Evolution of STEMI
A. Normal
B. Hyper-acute T-waves: Minutes
to Hours
C. ST-Elevation: 0-12 Hours
D. Q-Wave Development: 1-12
Hours
E. ST-Elevation with T-wave
inversion: 2-5 days
F. T-Wave recovery: weeks to
months
74. REVIEW OF EKG COMPLEXES
BACK TO BASIC DYSRHYTHMIA
INTERPRETATION
At least it’s not Acid-Base Balance!
75.
76. QRS
Q wave:
• First negative deflection, usually preceding an R wave
R Wave:
• First positive deflection
S Wave:
• Negative deflection following an R wave
79. T Wave
Large wave form following QRS Complex
Represents Ventricular Repolarization
Should be upright in most leads (III and V1)
Look for consistent morphology
81. T-P Segment
Area between, yup you guessed it, the end of
the T-Wave and the beginning of the P-Wave
Indentify this area and use it as your point of
reference for ST Segment Deviation
T-P Segment becomes your isoelectric line
83. ST Segment
The segment immediately following the QRS
complex and ending at the T wave
The J point (junction point) is the exact point
where the QRS stops and the ST begins
85. ST Segment
The ST segment is normally level with the T-P
segment rather than the PR segment
Examine every lead for ST segment elevation
of 1 mm or more.
1998
85
88. Myocardial Infarction Labels
For pre-hospital purposes
Non- ST- Elevation MI (NSTEMI) = Non-Q-Wave MI
(NQMI)
ST Elevation MI (STEMI) = Q-Wave MI (QMI)
93. ST Segment Elevation
Indicators to look for:
• Injury
• ST segment elevation >1 mm (>2 mm in septal leads)
• Present in two or more related or anatomically
contiguous leads
• Measure at J point (plus 20 - 40ms) to baseline
94. ST Segment Elevation - continued
ST elevation means
acute transmural injury
• Involves three layers of
the heart
In an acute MI, the
shape is not as
diagnostic as
• Reciprocal changes
• Patient history
• Presentation
96. ST Depression
The causes of ST depression
• Reciprocal changes to ST elevation
• Ischemia or subendocardial injury
• Certain medications, such as digitalis
If ST segment depression does not appear to
be reciprocal
• Could be myocardial ischemia or injury to the
subendocardial wall
• Involves a single layer of the heart muscle.
98. Inverted T Waves
One early sign of an ACS and MI is the T-
Wave Inversion
Because at times, the ST changes may
disappear as the area is reperfused by NTG, a
baseline 12 Lead prior to the administration of
NTG can be helpful.
99. Inverted T Waves - continued
Key points about
inverted T Waves
• Can represent Ischemia
(transient reduction in
blood flow)
• Symmetrical inverted T
waves in two or more
related leads
• Inverted T waves normal
in Leads VI and III
100. Pathological Q Wave
Signifies infarction, or
death of the tissue
Indicators of an
Infarct
• Pathological Q wave
• >40 ms, or 0.04 sec
wide, or 1/3 of R wave
height
• Indicates on-going or
permanent damage
105. Frequency Response
Monitor frequency ranges eliminate artifact at
the expense of ST-T accuracy
Do not rely on monitor quality tracings for
diagnostic interpretation
120. ST Segment Elevation in Leads?
Reciprocal ST Segment Depression in Leads?
Make Sense?
121. ST Segment Elevation in Leads: ____________________________
Reciprocal Changes in Leads: ____________________________
ST Segment Elevation in Leads?
Reciprocal ST Segment Depression in Leads?
Make Sense?
122. ST Segment Elevation in Leads?
Reciprocal ST Segment Depression in Leads?
Make Sense?
124. Computerized Interpretive Statement
In existence for over 50 years
Statistically accurate
Not always correct
MUST ALWAYS BE VIEWED IN LIGHT OF THE
SURROUNDING CLINICAL CIRCUMSTANCES
125. 12 Lead ECG Interpretive Algorithms
It is important to note that there are several 12
Lead ECG Interpretive Algorithms used in
EMS transport monitors
• GE (Marquette) 12SL Interpretive Algorithm
• ZOLL M, CCT, and E Series
• Physio Control Lifepak 12
• Inovise 12 L Interpretive Algorithm
• ZOLL X Series, Propaq MD
• Glasgow 12 Lead Analysis Program
• Physio Control Lifepak 15
• Philips DXL 12 Lead Algorithm
• Philips MRX
126. Acute Myocardial Infarction Statements
***Acute MI***
***STEMI***
***Meets ST Elevation MI Criteria***
98% - 99% specificity
52% - 70% sensitivity
Acute MI Statements = STEMI
127. Sensitivity
Refers to recognition
If the test always recognizes the disorder,
sensitivity would be 100%
False negatives are failures of sensitivity
A false negative occurs when the condition
exists but the test fails to find it
128. Specificity
Refers to the number of diagnoses confirmed
If the diagnosis were corroborated every time
the test identifies it, it would be 100% specific
False positives are failures in specificity
A false positive occurs when the test indicates
the disease is present, when in fact it is not
129. ACS Risk Factors
Diabetes
Smoking
Hypertension
High Cholesterol
Family History
Obesity
Sedentary Life
130. ECG Subsets for ACS
Non-Diagnostic
Suspicious for Ischemia
Suspicious for Injury
132. Interpretive Statement
For Non-Diagnostic ECGs
No ST/T abnormality statements
May point out other abnormalities such as chamber
hypertrophy, axis deviation, etc.
May point out old Q wave MIs without ST-T
abnormalities
133. Non-Diagnostic ECG
Does not rule out ACS
Look in additional leads if story is strong and or risk
factors high
Look for non-cardiac causes of symptoms
Repeat ECG often, it may change
134. Suspicious for Ischemia
ST & T wave abnormality, possible anteriolateral ischemia
ST & T wave abnormality, possible inferior ischemia
Abnormal ECG
ST & T wave abnormality, possible anteriolateral ischemia
ST & T wave abnormality, possible inferior ischemia
Abnormal ECG
135. Suspicious for Ischemia
Abnormal ST segment depression and/or T wave
inversion
Absence of ST Elevation
May represent UA or NSTEMI
136. Suspicious for Ischemia
Unstable Angina (UA) or Non-ST Elevation MI
(NSTEMI) ?
Cardiac Markers will make the differentiation
Pre-treatment ECG useful
Repeat the ECG often
137. The History
Good Assessment
• HPI
• Nature of Symptoms
• OPQRST
• Patient History
Traditional Risk Factors
• Age
• Male Sex
• DM
• Tobacco
• History of CAD
• Family History
• HTN
• Cholesterol
Non-Traditional
Risk Factors
• DM = CAD
• HIV with or without
HAART
• Cocaine/Meth
• CRI
• SLE
140. Special Consideration
ST depression in early V leads
• May be anterior ischemia
• May be reciprocal changes of posterior MI
• Check V7-V9 for ST elevation
Move to Acute MI category if ST Elevation
present in V7-V9
141. Sinus rhythm with first degree AV block with occasional supraventricular complexes
Possible left atrial enlargement
Inferior infarct
Marked ST depression consistent with subendocardial injury
**Acute MI**
Sinus rhythm with first degree AV block with occasional supraventricular complexes
Possible left atrial enlargement
Inferior infarct
Marked ST depression consistent with subendocardial injury
**Acute MI**
Suspicious for Injury
142. Suspicious for Injury
ST Elevation
2 or more anatomically contiguous leads
1 mm or more
143. ECG Subsets
Pathological Q Waves
Q waves may appear with acute or old infarcts
Older infarcts will display Q waves without ST-T
abnormalities causing computer to note infarct
Do not confuse infarct statement with
***Acute Myocardial Infarction*** statements
146. History of RVI
Right Ventricular Infarctions (RVI) were initially
described 70 years ago.
It wasn’t until 1974 before the significance of
the RVI was truly understood.
Before 1974 cardiologists believed that the
right ventricle was not an essential component
of adequate circulation.
147. Epidemiology
RVI accompany extensive inferior-posterior
wall MIs.
Risk factors include chronic lung disease, and
right ventricular hypertrophy.
RVI are difficult to diagnose.
Only 50% of patients will have hemodynamic
compromise.
148. Mortality and Morbidity
Inferior MIs with an associated RVI have
mortality rates that range between 30-50%
Inferior MIs without RVI involvement have a
6% mortality rate.
Patients with minimal Left Ventricle (LV)
involvement have excellent long term survival
151. Right Ventricle A & P
The RV has lower afterload, a lower oxygen
demand and a higher oxygen supply
It is relatively resistant to irreversible ischemic
damage during right coronary artery occlusion
Normal right ventricular end diastolic pressure
is between 2-4 mmHg
Right ventricle has the same CO as the left
ventricle 4-6 L/min
152. Left Dominant vs. Right Dominant
85% of the population is right dominant.
7.5% of the population is left dominant.
7.5% of the population is co-dominant.
Right dominant infers that the RCA supplies
circulation to the inferior portion of the
interventricular septum.
153. RVI Causes
There is right ventricle involvement in
approximately 33% of Inferior MIs
RVI occurs when there is an occlusion of the
RCA proximal to the acute marginal branches
in R dominant patients
RVI occurs with an occlusion of the left
circumflex artery in patients who are L
dominant
RVI can be caused by an occlusion of the LAD
but this is rare
Isolated RVI is rare – 2% of autopsies
154. RVI Causes
Right Side
Dominant -
occlusion above
the marginal
artery will cause
an RVI
Left Side
Dominant -
occlusion of the
Circumflex
Artery will
cause RVI
RVI indicates
a proximal
occlusion
and a serious
infarction
155. What Happens
Occlusion to the RCA happens above the
marginal branches
The right ventricle now becomes a conduit
It is unable to handle venous return
Resulting in decreased RV compliance,
decreased stroke volume, and decreased
cardiac output
156. Signs and Symptoms
Increased jugular venous pressure
Hypotension
• Before or after NTG administration
Clear lung fields
Kussmaul sign
Pulsus paradoxus
Cool, clammy skin
157. Chest Pain
Anginal (Ischemic) - Fullness, pressure,
crushing may radiate to neck, jaw, back, etc.
Atypical - Unilateral, sharp, changes with
position, pleuritic, muscular-skeletal, not in
chest but in jaw, neck, back
158. 12 Lead ECG Findings
ST segment elevation in inferior leads
Greater ST segment elevation in lead III than
lead II in an inferior wall MI
ST segment depression in leads V1-V4
• May be confused with anteroseptal MI.
Right bundle branch blocks and complete
heart blocks are the most common conduction
disturbances
159. Right Sided 12 Lead ECG
Complete right side 12 lead is preferable
V4R is the best single view
A 1 mm elevation in the ST segment is 70%
sensitive and 100% specific for a RVI
Elevation in this lead is transient and resolves
within 10-12 hrs
A right sided EKG should be done as soon as
possible on all inferior wall MIs
161. Right Sided Lead Placement
V3R - Between V1 and V4R
V4R - 5th ICS, right mid-clavicular line
V5R - Between V4R and V6R
V6R - Right mid axillary line, level with V4R
162.
163. Hemodynamic Consequences of RVI
Compensated
• Decreased R ventricular contractility
• Decreased blood flow to Left ventricle
• Decreased stroke volume
• Increased HR to maintain Cardiac Output
• Increased systemic vascular resistance
• Mildly reduced Cardiac Output
Decompensated
• Drastically reduced Cardiac Output
• Hypotension
• Increased blood volume in Right ventricle
• Decreased Right ventricular ejection
• Increased pressure in Right atrium and ventricle
168. Treatment
Early STEMI team activation and reperfusion
strategies
Oxygen
• Increases oxygen supply to the myocardium. (≥ 94%
SpO2)
Aspirin
• Decreases platelet aggregation
Fluids
• Volume loading with isotonic crystalloid is the initial
treatment for hypotensive patients suffering from a RVI
• Working on Starling’s Law
170. Treatment
The right ventricle is sensitive to beta adrenergic
stimulation and blockade
If the response to volume loading is not favorable
then a positive inotropic agent should be initiated
Dobutamine is the drug of choice and should be
titrated to maintain an adequate cardiac output
Other therapies should include:
–TCP initiation for significant heart blocks.
–Synchronized cardioversion for hemodynamically unstable
atrial fibrillation
171. Posterior Infarction
Occurs in about 33% of all inferior MI’s
Usually does not create the extraordinary
effects that an RVI does.
May present isolated from an inferior MI
Evidenced by ST segment elevation in Leads
V7, V8, and V9, with reciprocal depression in
Leads VI-V4.
172. Pure Posterior MI - Note ST depression in early V
leads. ST Elevation is present only in direct
posterior leads V7-V9.
173.
174. Acute Posterior - Lateral myocardial infarction
Hyperacute - The mirror image of acute injury
in leads V1 - V3 - Fully Evolved - Tall R wave,
tall upright T wave in leads V1 -V3 usually
associated with inferior and/or lateral wall MI
175. Posterior Lead Placement
V7 - Post axillary line, level with V4
V8 - Mid scapular line, level with V4
V9 - Left paravertebral area, level with V4
176. Misdiagnosis
Misdiagnosed Chest Pain is the single largest area of
litigation against Emergency Room Physicians. MACEP 2005
Patients with ACS may have chest wall tenderness on
palpation. MACEP2005
One survey included 600,000 patients diagnosed with
M.I. Study included 25% of all hospitals in US. One
question asked…
Did you have chest pain at any point?
33% of all patients survey answered “NO”
177. Misdiagnosis
Misdiagnosed Chest Pain is the single largest area of
litigation against Emergency Room Physicians. MACEP 2005
Patients with ACS may have chest wall tenderness on
palpation. MACEP2005
One survey included 600,000 patients diagnosed with
M.I. Study included 25% of all hospitals in US. One
question asked…
Did you have chest pain at any point?
33% of all patients survey answered “NO”
188. Introduction
A BBB is an electrical phenomenon
characterized by a widening of the QRS of at
least 0.12 seconds or greater
The wider the QRS complex, the lower the
patient’s Cardiac Output
189. Anatomy & Physiology
Blood supply for the bundle branches usually
comes from the left anterior descending
coronary artery, but also can be from the AV
nodal branch of the right coronary artery
Usually, depolarization is simultaneous with
the right and left ventricle, via the bundle
branches
192. Misdiagnosis
Although traditionally deemed as low risk:
• Pleuritic
• Sharp and stabbing pain,
• Pain reproducible with palpation or movement
• Pain that is either very short or prolonged in
duration
A significant number of patients diagnosed with M.I.
presented with these symptoms*
One study revealed that 7% of all M.I. patients
evaluated had pain that was fully reproducible on
palpation*
*Lee TH, Cook EF, Weisberg M, et al Acute chest pain in the ED, Arch
Internal Med.
193. Diagnosing BBB’s
V1 is the lead to use to diagnose BBB’s
This lead looks across the ventricles and can see both
bundle branches
To diagnose bundle branch blocks, use the turn signal
criteria
First – find a supraventricular complex
• Associated P wave
• Greater 0.12 sec
Next – find the J point, the point in which the QRS
turns into the ST segment
Then – look at the direction from which the QRS
terminates
• If the complex comes from above – then it is a RBBB
• If the complex comes from below – then it is a LBBB
194.
195. LBBB is identified by a wide QRS
with the terminal portion of the
QRS being negative in V1
LBBB is identified by a wide QRS
with the terminal portion of the
QRS being negative in V1
Left Bundle Branch Block
196. RBBB is identified by a wide
QRS with the terminal
portion of the QRS being
positive in lead V1
RBBB is identified by a wide
QRS with the terminal
portion of the QRS being
positive in lead V1
V1
Right Bundle Branch Block
197. Significance of BBB
In the presence of an AMI, a BBB is a serious
complication that usually indicates extensive
coronary artery occlusion and anterior wall
damage
BBB complication of an MI has a mortality rate
4x greater than those with MI alone
Typically occurs with occlusions to the left
anterior descending coronary artery
• Septal or anterior wall MI’s
• Frequently develop BBB’s or CHB
198. Significance of BBB - continued
The presence of an LBBB obscures the ST
segment, making ECG diagnosis of an AMI
very difficult
With RBBB, the ST segment is intact, and MI
determination is easier
When a partial LBBB (fasicular) is combined
with an RBBB, it is called a bifascicular block
When a bifascicular block exists,
antiarrythmics, and morphine can slow the
conduction system through the ventricles,
resulting in drug-induced CHB, or possibly,
ventricular asystole
199. The Joys of a LBBB
May be new or old
If not proven to be old it is presumptively
new
AHA Guidelines state that patients with a
new or presumably new BBB are placed in
the same category as patients with STEMI
Why?
Because changes that occur with LBBB
mask ST Segment changes
200. AHA MI Consensus Statement 2013
New or presumably new LBBB at presentation
occurs infrequently, may interfere with ST-
elevation analysis, and should not be
considered diagnostic of acute myocardial
infarction (MI) in isolation
201. MONA for all ACS patients?
Morphine
Oxygen?
NTG
ASA
12 Lead EKG
Transport Dx!
Beta Blockers?
202. MONA for all ACS patients?
Morphine
Oxygen?
NTG
ASA
12 Lead EKG
Transport Dx!
Beta Blockers?
203. MONA for all ACS patients?
Morphine
Oxygen?
NTG
ASA
12 Lead EKG
Transport Dx!
Beta Blockers?
204. In LBBB, leads with negative
QRS deflection will display ST
elevation and an upright T wave
In LBBB, leads with negative
QRS deflection will display ST
elevation and an upright T wave
Leads with positively deflected
complexes will display ST
depression and negative T
Waves
Leads with positively deflected
complexes will display ST
depression and negative T
Waves
ST-T Discordance
206. Normal sinus rhythm with frequent
premature ventricular complexes
Left axis deviation
Left Bundle branch block
Normal sinus rhythm with frequent
premature ventricular complexes
Left axis deviation
Left Bundle branch block
Note the ST-T discordance—it
also occurs with PVCs
ST-T Discordance
207. Sgarbossa’s Criteria
The three criteria Sgarbossa's criteria are:
• ST elevation ≥1 mm in a lead with a positive QRS
complex (ie: concordance) - 5 points
• ST depression ≥1 mm in lead V1, V2, or V3 - 3 points
• ST elevation ≥5 mm in a lead with a negative
(discordant) QRS complex - 2 points
≥3 points
• 90% specificity of STEMI (sensitivity of 36%)
208. Other Criteria
ST elevation more than you'd expect from
LBBB alone
• Must be present in 2 or more contiguous leads - (e.g.
> 5 mm in leads V1 - V3)
209.
210. Acute myocardial infarction in the
presence of Right Bundle Branch Block
Features suggesting acute septal-
anterior MI
ST changes not obscured by RBBB
211.
212. Therapy: What does it get me?
Aspirin
• 21-25% reduction if given during ACS and continued
out 35 days (ISIS-2, JACC 1988)
Beta-blocker
• Clearly shown to reduce all-cause mortality long term
following ACS
• Possible 1% reduction in re-infarction and VF is offset
by the 1.1% of patients who end up in cardiogenic
shock when it is inappropriately given
(COMMIT/CCS-2, 2005)
213. Hemodynamic Effects of BBB’s
In some cases, a BBB can have a significant
hemodynamic effect
A BBB means a delayed conduction and
depolarization time
QRS greater than 0.17 seconds, have an
Ejection Fraction (EF) of less than 50%
• Normal is 55% - 75%
Contractility is compromised, hence CO is
affected
215. Determining Axis and Hemiblock
Axis: defined as the general direction of
electrical impulses travel through the heart
• As they travel, they are carried in different directions
• 90% of the impulses cancel one another out
• The remaining 10% travel in one primary direction
• Assessing the direction of these impulses provides
clues about the severity of a patient’s condition and
helps to guide treatment
216.
217. Hexaxial System
Includes limb Leads I,
II, III and the
augmented Leads
aVL, aVR, and aVF.
The result is like a pie
of six equal pieces
and lines to which
you add in the
degrees.
218. Normal Axis
To determine axis –
run Leads I, II, III
Normally, electrical
impulses start from the
SA Node, and travel
downward to the lower left
side of the heart
Conducted impulses
travel toward the positive
electrodes in Lead I, II, III,
creating an upward QRS
deflection.
219. Left-Axis Deviation
Axis is rotated to the left
Two different categories -
Physiological left-axis deviation (normal
variant)
• Upward deflection in Lead I, Upward or Isoelectric
Deflection in Lead II, and a Negative deflection in
Lead III.
Pathological left-axis deviation
• Upward deflection in Lead I, Negative deflection in
Lead II and III.
221. Right-Axis Deviation
In some patients, the axis may be deviated to
the right
In children, this is a normal variant
In adults, a right-axis deviation has
• Negative deviation in Lead I
• Positive deviation in Lead III
• Lead II can be positive, negative, or isoelectric
224. Hemiblock
Best defined as a block of one of the two
fascicles of the left bundle branch system.
There is a right bundle branch and a left
bundle branch that divides into separate
fascicles, also known as hemifascicles.
The hemifascicles are known as the left
anterior and left posterior, those combined with
the right right bundle branch make up a
trifascicular system.
225. Hemiblock - continued
Impulses can travel in three ways to the
ventricles:
• Right Bundle Branch
• Left Posterior Hemifascicle
• Left Anterior Hemifascicle
Blocks in this system can be a precursor to
heart blocks
Can help determine which patients are at risk
for complete heart blocks
In presence of MI, 4 times higher mortality
rate than an MI without a hemiblock
226. Left Anterior Hemiblock
Occurs when the anterior fascicle of the LBB
system becomes blocked
A pathological left-axis deviation is indicative
of an anterior fasicular block
• Other clues:
• Small Q wave in Lead I
• Small R wave in Lead III
• Can have a narrow QRS complex
LAD branch of the left coronary artery provides
blood supply for the anterior hemifascicle
4 times higher than an MI without an
anterior hemiblock
227. Left Posterior Hemiblock
Occurs when the posterior fascicle of the LBB
system is blocked
A right-axis deviation is indicative of a left
posterior hemiblock
• Other clues:
• Small R wave in Lead I, small Q wave in Lead III
The clinician should also inspect for the presence of:
• Right ventricular hypertrophy
• JVD, Pedal edema and patient history
228. Left Posterior Hemiblock - continued
The posterior hemiblock is considered more
acute than the anterior hemiblock
The posterior hemifascicle is thicker than the
anterior hemifascicle, having more cells and
needing a more significant supply of blood
A redundant blood supply is required from two
different coronary arteries:
• Right coronary artery
• Circumflex
If both coronary arteries are blocked, extensive
coronary occlusion has occurred
229. Clinical Significance of Hemiblock
The clinical significance of hemiblock can be
summarized as follows:
• Four times higher mortality rate for patients having an
AMI with a hemiblock than those without hemiblock
• Significantly higher risk for complete heart block
• In the setting of an AMI, can indicate proximal artery
occlusion
231. Relationship Between DBT and Mortality
Deluca G et al. Time delay to treatment and mortality in primary angioplasty for AMI: every
minute of delay counts. Circulation 2004; 109(10): 1223-1225
30 minute delay
= 7.5% increase
in mortality!
232. The Chart and a 3 or 4 Lead ECG
Look at Leads I, II and III
Determine whether the QRS complex is more
positively or negatively deflected in each lead.
Compare your findings with the Chart to
identify the axis and hemiblock.
233.
234. Calculated Axis Angle
The number to look
for is the R axis or
QRS axis
The computerized
measurements can
be used to identify
the axis deviation
236. Right Atrial Abnormality
Right Atrial Enlargement
(RAE) will show tall,
pointed P waves in the
inferior leads, II, III,
aVF.
The P wave will be
more than 2.5 mm
3-P memory aid
• Pointed
• Prominent
• Pulmonary
237. Right Atrial Enlargement
Most likely causes
• Congenital heart disease
• Tricuspid or pulmonary valve disease
• Pulmonary hypertension
Clinical implications
• Generally not an acute problem
• Frequently seen with Right Ventricular Hypertrophy
238. Left Atrial Abnormalities
Left Atrial
Enlargement (LAE)
Most common cause
is LVH
ECG criteria
• Lead II widened p wave
(>120 ms, or 3mm) with
a notched or m-shaped
appearance
• Lead V1 broad terminal
negative P deflection of
more than 1 mm
239. Right Ventricular Hypertrophy
Caused by increased pressure, or volume in
the right ventricle
Generally occurs in circumstances similar to
those for RAE
RVH is characterized by large forces that go
away from the lateral leads and towards V1
ECG Criteria for RVH
• Right Atrial Enlargement
• Narrow QRS
• Right axis deviation
• R Wave height in V1 greater than 7mm
• Asymmetrical down sloping ST segment in inferior leads
240. Value of an Early ECG
ECG changes from ACS are dynamic
MONA treatment may mask changes
ST elevation = reperfusion indication
EMS is in a privileged position
• Early 12-lead
• During symptoms
• Before medication
241. Value of an Early ECG
ECG changes from ACS are dynamic
MONA treatment may mask changes
ST elevation = reperfusion indication
EMS is in a privileged position
• Early 12-lead
• During symptoms
• Before medication
242. Left Ventricular Hypertrophy
Clinical implications
• Higher incidence of sudden death or ischemic
arrhythmias
• Can mimic the ST depression or elevation seen with
myocardial ischemia
• May be caused by an AMI
• In the presence of an LBB, LVH criteria almost
impossible to differentiate
• May be a useful clue as to hemodynamic condition
244. Potassium - Hypokalemia
Hypokalemia
• Serum levels below 3.5 mEq/L
• Most commonly caused by vomiting, diarrhea,
diuretics, and gastric suctioning
• Muscle weakness and polyuria are common signs
and symptoms
• Digitalis resulting from hypokalemia, causing serious
dysrthythmias, ie: torsades
• A-flutter, heart blocks, and bradycardia
245. Potassium - Hypokalemia
ECG Changes
• ST segment depression
• T waves flattened or joined
with U waves
• U waves getting larger
than the T waves as the
potassium level falls
• QT interval appearing to
lengthen as T combines
with U
• PR interval increases
246. Potassium - Hyperkalemia
ECG Changes
• Mild cases – less than 6.5 mEq/L
• Tall, tented, peaked T waves with a narrow bases
• Best seen in Leads II, III, V2, and V4
• Normal P waves
• Moderate cases – less than 8 mEq/L
• QRS widens
• Broad S wave in V leads
• Left-axis deviation
• ST segment is gone, contiguous with peaked T wave
• P wave starts to flatten and diminish
253. QT Interval
Represents the time from the start of
depolarization of the ventricles to the end of
repolarization
QT interval is measured from the start of the
QRS to the end of the T wave
QTc is represents the corrected QT interval for
the current heart rate
254. Reduce Time to Thrombolysis
Many studies have shown significant
reductions in hospital-based time to
treatment with fibrinolytic therapy in
patients with AMI identified before arrival
by 12-lead ECG. Time savings ranged from
20-55 minutes.
AHA, Guidelines 2000
255. Reduce Time to Thrombolysis
Many studies have shown significant
reductions in hospital-based time to
treatment with fibrinolytic therapy in
patients with AMI identified before arrival
by 12-lead ECG. Time savings ranged from
20-55 minutes.
AHA, Guidelines 2000
258. Pericarditis
ECG clues
• ST Segment elevation
• Concave in almost all leads, except aVR and V1
• T wave elevation starting above the isolectric line
• ST segment depression, or T wave inversion
262. Wolf-Parkinson-White (WPW)
Caused by accessory pathway between Atria
and Ventricles.
Pathway known as the Bundle of Kent
Classic signs
• Delta Wave
• Short P-R Interval
265. Bradley EH, et al. N Engl J Med. 2006. November 13. [Epub ahead of print].
Strategies Associated With a Significant
Reduction in Door-to-Balloon Time
Strategy
Mean reduction in
door-to-balloon
time (min)*
Having emergency physicians activate the cath lab 8.2
Having single call to a central page operator activate cath lab 13.8
Having the ED activate the cath lab while patient still en route 15.4
Expecting staff to arrive at cath lab within 20 minutes after
page
19.3
Having an attending cardiologist always on site 14.6
Having staff in ED and cath lab use and receive real-time
feedback
8.6
267. Takotsubo Cardiomyopathy
Also known as:
• Transient apical ballooning syndrome
• Stress-induced cardiomyopathy
• Gebrochenes-Herz Syndrom
• Broken heart syndrome
Can be triggered by:
• Emotional stress
• Death of a loved one
• Divorce or break up
• Constant anxiety
• Physical Stressor
• Asthma attack
• Sudden illness
268. Takotsubo Presentation
EMS and E.D. presentation
• Chest pain with or without dypsnea
• ECG changes mimicking anterior AMI (V2-V5)
• Sudden onset of congestive heart failure
• Moderate cardiac enzyme elevation
Invasive evaluation and enhanced imaging
• Bulging of the left ventricular apex
• Hypercontracile base of the left ventricle
• No significant coronary artery blockages on
angiogram
Takotsubo Cardiomyopathy is found in
1.7% – 2.2% of all ACS patients
272. Treatment and Prognosis
Treatment includes
• ASA
• NTG for Chest Pain
• Fluids
• Negative inotropes
• Calcium Channel Blockers, Beta Blockers, ACE Inhibitors
• Intra-aortic balloon pump support
• Cautious use of positive inotropic agents
Symptom resolution
• LV function improvement in first few days
• Normalization in first few months
Mortality rate 0 - 8%
273. Brugada Syndrome
Caused by a genetic disorder
Characterized by ECG changes and an
increase risk of Sudden Cardiac Arrest (SCA)
ECG changes
• Typically V1 - V3
• ST segment elevation
• RBBB like appearance
Most common cause of SCA in young men
without underlying cardiac disease in Thailand
and Laos
278. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
279.
280. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
281.
282. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
283.
284.
285.
286. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
287.
288. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
289.
290. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
291.
292. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
293.
294. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________
295.
296. ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________