STEMI Training

12 Lead EKG Interpretation
and STEMI Management

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

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

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.

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!

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

Acute Coronary Syndromes
Unstable Angina (UA)
Non-Q Wave Myocardial Infarction (NQMI)
Q Wave Myocardial Infarction (QMI)

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)

ACS Risk Factors
 Diabetes
 Smoking
 Hypertension
 High Cholesterol
 Family History
 Obesity
 Sedentary Life

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

Chief Complaints in ACS
 Chest Pain
• Anginal
• Atypical
 Anginal Equivalents

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

Anginal Equivalents
 Dyspnea
 Syncope
 Diaphoresis
 Weakness, nausea, vomiting
 Palpitations, dysrhythmias
 Other

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”

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.

MONA for all ACS patients?
Morphine
Oxygen?
NTG
ASA
12 Lead EKG
Transport Dx!
Beta Blockers?

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)

ECG: First Priority
Then make a destination decision…
…STEMI = PCI Center

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!

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

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

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

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

 Clip chest hair
• Faster
• More comfortable
• Prevents infection
• Safer (less nicks and cuts)
 Shaving is acceptable alternative
• Think gross decon
• Not Remington close

 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!

 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

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

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

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)

Indicative Leads
 Positive Pole (+)
 Acts as point of reference
 Imagine the positive pole as a camera lens

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

Ward and Wayne’s First Marketing Project

Distal Lead Placement
 If you are still using the machine from the
previous slide, then yes, distal lead placement
is required

Indicative Lead Groups
 Inferior Wall - II, III, and aVF
 Septal Wall - V1, V2
 Anterior Wall - V3, V4
 Lateral Wall - V5, V6, I, and aVL

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.

Specialty Leads
 Posterior Wall - V7-V9
 Right Ventricle - V3R-V6R

Survey Says
 ST elevation in the inferior leads
 II, III and aVF
 Acute inferior myocardial infarction

Oh Boy!
 ST elevation in the septal, anterior and lateral
leads
 V1 - V6, I and aVL
 Acute anterior-lateral myocardial infarction

CORONARY PERFUSION
ANATOMICAL REVIEW

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.

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

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

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

ST depression T wave inversion

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

REVIEW OF EKG COMPLEXES
BACK TO BASIC DYSRHYTHMIA
INTERPRETATION
At least it’s not Acid-Base Balance!

QRS
 Q wave:
• First negative deflection, usually preceding an R wave
 R Wave:
• First positive deflection
 S Wave:
• Negative deflection following an R wave

> 1mm < 1mm
Pathological Physiological
Q Waves

T Wave
 Large wave form following QRS Complex
 Represents Ventricular Repolarization
 Should be upright in most leads (III and V1)
 Look for consistent morphology

UprightUpright InvertedInverted
T Waves

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

T-P SegmentT-P Segment BaselineBaseline
T-P Segment

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

Isoelectric Elevated Depressed
ST Segment

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

ST Elevation in Leads II, III, aVF
Practice Sample

T Wave Inversion
Practice Sample

Pathological Q’s in II & III ??
Practice Sample

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

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

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.

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.

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

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

COMPONENTS OF THE
12 LEAD EKG
What is the box trying to tell us?

Frequency ResponseFrequency Response

Frequency Response
 Monitor frequency ranges eliminate artifact at
the expense of ST-T accuracy
 Do not rely on monitor quality tracings for
diagnostic interpretation

Monitor Quality Diagnostic Quality

One Complete Cardiac CycleOne Complete Cardiac Cycle

Patient
Information
Patient
Information
MeasurementsMeasurements
Computerized Interpretive
Statement
Computerized Interpretive
Statement

ACUTE INFARCT LOCALIZATION
Practice

ST Segment Elevation in Leads?
ST Segment Depression in Leads?
Interpretation/Localization?

II, III, aVF
I, aVL, V2 - V4
I, aVL, V2 - V4
None
Acute Inferior Wall MI

V1-V4, (aVL?)
II, III, aVF, V4, V5
III
V1
Acute Anteroseptal MI

V1 - V5, I, aVL
III
III
V1 - V5, II, III, aVF
Acute Extensive Anterior MI &
Old Inferior Wall MI

Reciprocal Changes
Inferior: II,III,aVF Anterior: V1-V6, aVL, I
Septal: V1, V2 Lateral: V5,V6, I, aVL
Early Anterior: V1-V3 Posterior: V7-V9

Reciprocal ST Segment Depression in Leads?
Make Sense?

ST Segment Elevation in Leads: ____________________________
Reciprocal Changes in Leads: ____________________________
Reciprocal ST Segment Depression in Leads?
Make Sense?

COMPUTERIZED
INTERPRETIVE STATEMENTS
The Computer Cardiologist

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

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

Acute Myocardial Infarction Statements
***Acute MI***
***STEMI***
***Meets ST Elevation MI Criteria***
 98% - 99% specificity
 52% - 70% sensitivity
Acute MI Statements = STEMI

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

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

ECG Subsets for ACS
 Non-Diagnostic
 Suspicious for Ischemia
 Suspicious for Injury

Non-Diagnostic ECG
Normal sinus rhythm
Normal ECG
****Unconfirmed****
Normal sinus rhythm
Normal ECG
****Unconfirmed****

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

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

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

 Abnormal ST segment depression and/or T wave
inversion
 Absence of ST Elevation
 May represent UA or NSTEMI

 Unstable Angina (UA) or Non-ST Elevation MI
(NSTEMI) ?
 Cardiac Markers will make the differentiation
 Pre-treatment ECG useful
 Repeat the ECG often

High-Risk Management
 Repeat ECG
 Heparin
 GPIIb/IIIa inhibitors
 Integrilin (eptifibatide)
 Aggrastat (tirofiban hydrochloride)
 Beta blockers or calcium channel blockers
 IV Nitrates
 Early coronary intervention

Interpretive Statement
For Ischemic ECGs
 Non-specific ST/T abnormality statements
 Suspicious for ischemia
 Subendocardial injury pattern
 Localized ischemia statements

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

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

Suspicious for Injury
 ST Elevation
 2 or more anatomically contiguous leads
 1 mm or more

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

Sinus tachycardia
Inferior infarct
Abnormal ECG
Sinus tachycardia
Inferior infarct
Abnormal ECG
Q Waves

RIGHT VENTRICULAR
INFARCTION
&
POSTERIOR WALL INFARCTION

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.

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.

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

Right Ventricular A & P
150
Right Ventricle
Left Ventricle

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

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.

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

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

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

Signs and Symptoms
 Increased jugular venous pressure
 Hypotension
• Before or after NTG administration
 Clear lung fields
 Kussmaul sign
 Pulsus paradoxus
 Cool, clammy skin

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

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

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

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

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

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

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.

Pure Posterior MI - Note ST depression in early V
leads. ST Elevation is present only in direct
posterior leads V7-V9.

 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

Posterior Lead Placement
V7 - Post axillary line, level with V4
V8 - Mid scapular line, level with V4
V9 - Left paravertebral area, level with V4

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

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

Ventricular Conduction in LBBB
+
1
3
2
V1
120 m/sec
1
2
3

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

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

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

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

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

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

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

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

Elevation Depression
Discordant Concordant Discordant Concordant
ST-T Discordance

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

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%)

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)

 Acute myocardial infarction in the
presence of Right Bundle Branch Block
 Features suggesting acute septal-
anterior MI
 ST changes not obscured by RBBB

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

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

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.

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.

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.

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

Right-Axis Deviation - continued

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.

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

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

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

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

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

RAPID AXIS AND HEMIBLOCK
CHART

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.

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

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

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

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

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

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

ELECTROLYTE, DRUG AND
OTHER ECG CHANGES

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

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

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

Potassium - Hyperkalemia
 Severe Cases
 Greater than 8 mEq/L
• P wave disappear
• Sine waves

Calcium
 Hypercalcemia is
suggested by a
shortened QT interval
 Hypocalcemia is
suggested by a
prolonged QT interval

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

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

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

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

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

Takotsubo vs. Normal
Takotsubo – Japanese octopus pot

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%

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

ST Segment Elevation in Leads: ____________________________
ST Segment Depression in Leads: ____________________________
Interpretation/Localization: ____________________________

Acknowledgements
 David Lacaillade
 Eric Kessler
Thanks!

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