12 Lead EKG 101
A Basic Overview of How to
Interpret 12 Lead EKGs and
Treat a Cardiac Patient
Region IV Pre-Hospital Systems Coordination Committee
Purpose:
The purpose of this course is to
provide pre-hospital clinicians with the
tools necessary to identify the basic
A&P of the heart, interpret 12 Lead
EKGs, localize and treat AMIs as well
as recognize imposters and potential
complications.
Basic Cardiac Anatomy &
Physiology
•Muscular pump about the size of your fist
•primary function is to pump oxygenated blood to the rest of the
body.
•Made up of four chambers,
•right and left atria
•right and left ventricles
•The septum is a thin muscular wall that separates the right and left
sides of the heart.
•Each contraction of the heart occurs in response to an electrical
impulse that starts in the upper portion of the heart.
•Blood is moved in a closed circuit through the body by the pumping of
the heart.
Basic Cardiac Anatomy &
Physiology
•The heart contracts and pumps blood out to the body (systole) and
relaxes to fill with more blood (diastole).
•The heart muscle itself is like all other organs in the body and
requires oxygen to function.
•The oxygen-rich blood is circulated to the heart muscle through the
coronary arteries.
•There are two main arteries:
•Right coronary artery
•Left main coronary artery
•both start at the aorta
• These vessels then branch off into smaller and smaller vessels
along the surface of the heart.
In order to perform work, the heart
needs oxygen and nutrients.
•There are two main arteries:
•Right coronary artery (RCA)
•Left coronary artery (LCA).
•The left coronary artery divides into:
•Left anterior descending (LAD)
branch
•Left circumflex branch(LCX)
•The right coronary artery and the
branches of the left coronary artery
provide numerous smaller branches
which penetrate the heart muscle,
supplying it with blood.
•Both coronary arteries originate
from the aorta and run along the
surface of the heart.
•In the majority of human hearts,
coronary circulation follows a
predictable pattern.
Left Main Coronary Artery
Branches quickly into the LAD & LCX.
Involves almost 2/3 of the heart muscle
Right Coronary Artery (RCA)
The RCA supplies blood to the bottom
(inferior) portion and part of the back
(posterior) portion of the left ventricle. The
posterior portion of the septum is also
supplied with blood from the RCA.
•SA Node 55%
•AV Node 90%
•AV Blocks
Left Anterior Descending Branch (LAD)
The LAD supplies blood to the front (anterior)
portion of the left ventricle, apical including
most of the anterior portion of the septum
separating the ventricles.
•Bundle Branch Block, AMI, CHF
Left Circumflux Branch (LCX)
The LCX supplies blood to the left side
(lateral) portion and the back
(posterior) portion of the left ventricle.
•SA Node 45%
•AV Node 10%
•Lateral & posterior MI
•Sino-Atrial (SA) Node: natural cardiac
pacemaker. The heartbeat starts here and
spreads throughout the network of
conduction fibers in the two atria causing
them to contract.
•Normally, the heartbeat can only reach the
ventricles (the two lower chambers), after it
has passed through the atrioventricular (AV)
node.
•Atrioventricular (AV) Node: slows down
the electrical signal so that the atrial
contractions can finish filling the ventricles
completely. The AV node also prevents the
lower chambers from beating too fast if the
atria develops a fast rhythm
(tachyarrhythmia).
•His Bundle, bundle branches, and
the Purkinje system : The electrical
signal finally passes to the ventricles
causing the ventricles to contract
Anatomy of an EKG
The EKG, or a measure of this electrical activity of
the heart, is comprised of 3 primary parts...
1. P wave---electrical depolarization of the
atria...contraction follows...
2. QRS COMPLEX---electrical depolarization of the
ventricles...contraction follows...
3. T wave---electrical repolarization of the
ventricles...and thus, relaxation...
P wave: Represents positive and negative deflections of
atrial contraction and relaxation
PR Interval: Distance between the P wave and the R
wave. Should be consistent
QRS Complex
Q wave: First negative deflection
•Normal in I, aVL, V1, V6
•Significant or pathologic is one box wide and/or 1/3
the height of the R wave
R Wave: First positive deflection
S Wave: Next negative deflection
ST Segment: Essentially isoelectric, slopes gentely upward
J point: the point at which the ST Segment takes off from
the QRS complex
T Wave: Upright always in leads I, II, V2-V6. aVR is always
negative. Leads III, aVL, aVF, and V1 can be positive or
negative
U Wave: Seen best in V3, same polarity as T wave, sign of
hypokalemia
QT Interval: One complete ventricular cycle. None are > ½
the preceding R-R
Putting the A&P with the EKG
Einthoven’s Triangle
Lead I
extends from
the right to the
left arm
-
+
Lead III
extends from the left
arm to the left foot
Lead II
extends from the
right arm to the
left foot
+
Anatomy of a 12-Lead EKG
This is an example a 12-lead EKG.
Anatomy of a 12-Lead EKG
(cont.)
•At the bottom of this 12lead are rhythm strips
(highlighted).
•Any of the 12-leads can
be shown as rhythm
strips.
•You can configure the
device to show you any
of the six limb leads on
the rhythm strip (I, II, III,
aVR, aVL or aVF).
Anatomy of a 12 Lead EKG
(cont.)
The format of the 12-lead EKG is very standard.
While there are a few exceptions, the format you see
here is typical of what you will see in most 12-lead
EKGs done in North America.
Anatomy of a 12-Lead EKG
(cont.)
•The 12-lead can provide a computer generated interpretation.
•When you see “ACUTE MI SUSPECTED” the machine is right about
98% of the time.
•In order to attain specificity, if the computer isn’t absolutely sure that
an AMI is present, it will not say anything about it.
•In other words YOU are the primary interpreter, the computer is your
backup.
Anatomy of a 12-Lead EKG (cont.)
•The 12-Lead is very good at measuring intervals and durations.
•It is better at measuring the PR-interval and the QRS width.
•We express these intervals and durations in seconds
•12-lead expresses them in milliseconds. It is simple to convert
milliseconds to seconds.
Anatomy of a 12-Lead EKG
(cont.)
•When you use an EKG to
determine the cardiac
rate and rhythm, certain
sampling time is required.
12-lead interpretation:
Only one beat from each
lead is needed to make an
interpretation.
Anatomy of a 12-Lead EKG
(cont.)
•There are six positive electrodes on the
chest, yielding six leads.
•There are four electrodes on the limbs
from which the EKG machine makes
another six leads.
•Each lead has one positive electrode.
•Positive electrode is a camera.
•view is from the positive electrode toward
the negative electrode.
•The portion of the left ventricle that each
leads “sees” is determined by the location
of that positive electrode.
•Different placements of the electrodes will
yield different viewpoints.
Anatomy of a 12-Lead EKG
(cont.)
Types of Leads
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Limb Leads
Chest Leads
Anatomy of a 12-Lead EKG
(cont.)
View of Posterior Heart Wall
•Leads V1 & V2
-Tall R
-ST Depression
-Upright T-Wave
Anatomy of a 12-Lead EKG
(cont.)
View of Inferior Heart Wall
• Leads II, III, aVF
- Looks at inferior heart wall
-Looks from the left leg up
Anatomy of a 12-Lead EKG
(cont.)
View of Lateral Heart Wall
• Leads I and aVL
– Looks at lateral heart
wall
– Looks from the left arm
toward heart
*Sometimes known as
High Lateral*
Anatomy of a 12-Lead EKG
(cont.)
View of Lateral Heart Wall
• Leads V5 & V6
– Looks at lateral heart wall
– Looks from the left lateral
chest toward heart
*Sometimes referred
to as Low Lateral or
Apical view*
Anatomy of a 12-Lead EKG
(cont.)
View of Entire Lateral Heart Wall
• Leads I, aVL, V5, V6
- Looks at the lateral wall of the
heart from two different perspectives
Lateral Wall
Anatomy of a 12-Lead EKG
(cont.)
View of Anterior Heart Wall
• Leads V3, V4
– Looks at anterior heart wall
– Looks from the left anterior
chest
Anatomy of a 12-Lead EKG
(cont.)
View of Septal Heart Wall
• Leads V1, V2
- Looks at septal heart wall
- Looks along sternal borders
Anatomy of a 12-Lead EKG
(cont.)
I Lateral
aVR
II Inferior
aVL Lateral
III Inferior
aVF Inferior
V1 Septal
V4 Anterior
V2 Septal
V5 Lateral
V3 Anterior
V6 Lateral
Anatomy of a 12-Lead EKG ST Segment
•The ST segment is normally isoelectric (baseline) neither elevated or
depressed.
•May slope upward toward
a relatively tall T wave
•The ST segment is probably the
single most important element to
identify on the ECG when looking for
evidence of AMI.
The Three I’s

Ischemia
– lack of oxygenation
– ST depression or T inversion

Injury
– prolonged ischemia
– ST elevation

Infarct
– death of tissue
– may or may not show in Q wave
CARDIAC ISCHEMIA
( Myocardial ischemia, Ischemic heart
disease, Ischemia, Myocardium ischemia,
Silent ischemia )
Cardiac ischemia is a situation in which the blood
flow within a coronary artery is limited to the
point where the oxygen needs of the heart muscle
cannot be met (hypoxia).
CARDIAC ISCHEMIA
Minor episodes of cardiac ischemia tend to cause
little long-term damage to the heart, but these
episodes can sometimes cause serious effects in
some patients:
 They can cause arrhythmias, which can lead to
either syncope or cardiac arrest and sudden
cardiac death.
 Severe or lengthy episodes can trigger a result in
myocardial infarction.
 The collective effects of minor episodes of
cardiac ischemia can potentially lead to
cardiomyopathy.
Symptoms of Cardiac Ischemia
May be painful
symptoms of cardiac
ischemia,
 Pain, pressure or
discomfort from
cardiac ischemia is
angina. Angina may
feel like a squeezing
vise or crushing
pressure deep in the
chest behind the
sternum. May also be
felt in the shoulders,
arms, back, neck or
jaw.
EKG in Acute Ischemia
Tracing taken during an episode of anginal pain
that occurred while the patient was at rest. Marked
ST elevation in leads V2-5 with some ST
depression in aVF.
EKG after Acute Ischemia
This tracing was taken 30 minutes after the initial.
The patient was pain-free and asymptomatic. The
ST segments are isoelectric, and the ECG is
normal
Evaluation after Acute
Ischemia

Subsequent clinical evaluation
– serial ECGs
– enzyme determinations,
revealed no evidence of acute myocardial
infarction. Disappearance of the ST elevation
and
the
absence
of
clinical
and
electrocardiographic evidence of infarction on
subsequent examinations indicate that initial
ECG is representative of severe, acute, and
reversible ischemia.
Well Perfused Myocardium
Epicardial Coronary Artery
Lateral Wall of LV
Septum
Left
Ventricular
Cavity
Positive Electrode
Interior Wall of LV
Normal ECG
Ischemia
Epicardial Coronary Artery
Lateral Wall of LV
Septum
Left
Ventricular
Cavity
Positive Electrode
Interior Wall of LV
Ischemia

Inadequate oxygen to tissue

Subendocardial

Represented by ST
depression or T inversion

May or may not result in
infarct
ST depression
Injury

Prolonged ischemia

Transmural

Represented by ST
elevation

Usually results in infarct
ST elevation
Injury
Thrombus
Ischemia
Infarct

Death of tissue

Represented by Q wave

Not all infarcts develop Q waves
Infarction
Infarcted Area
Electrically Silent
Depolarization
Many infarcts do not develop Q waves
Q Waves
Thrombus
Infarcted Area
Electrically Silent
Ischemia
Depolarization
Summary
A normal ECG does NOT rule out
ACS
 ST segment depression represents
ischemia

– Possible infarct
ST segment elevation is evidence of
AMI
 Q wave MI may follow ST elevation or
depression

Pathophysiology of the AMI
•Chronic accumulation of atherosclerotic plaque in
coronary vessels around the heart
•Fibrous plaque prone to rupture, lead to thrombytic
blockage
•Clots form due to damaged tissue and platelets
•Both release chemicals causing a clot to form
•Forms a substance called fibren that traps cells and
platelets eventually blocking and narrowing
•Tissue damage in AMI results from rupture of plaque on
vessel walls creating a chain reaction that forms a clot in
the coronary artery.
Process of an AMI
Impaired blood flow:
•Produces varying degrees of
myocardial injury
•Damage dependent on flow reduction
and duration
•Tissue death progress quickly in a
wave pattern
•Begins with endocardium
•Ends with epicardium
•Infarction becomes larger toward
the surface of the heart.
Ischemia – Shortage of oxygen at
cellular level
Injury – Diminishing supply of oxygen
Infarct – cardiac cells die of anoxia.
EKG Changes from Infarction
First Detectable Change in EKG
•Tall T-waves
•increase in height
•more symmetric
•may occur in the first few minutes
*Known as hyper acute phase*
EKG Changes from Infarction
“The Acute Phase”
Signs of Myocardial Injury
•ST Segment Elevation
•Primary indication of injury
•Occurs in first hour to hours
•ST Segment Elevation in Leads
•1mm or greater in limb leads
•2 mm or greater in chest leads
•Hallmark indication of AMI
*Known as Acute Phase*
EKG Changes of Infarction
“Reciprocal Changes”
ST elevation in contiguous leads most
often represents acute infarction
 ST depression in contiguous leads may
represent acute ischemia
 In acute infarction, ST elevation in
contiguous leads coupled with
reciprocal ST depression in noninfarcting leads is added evidence of an
AMI.

Reciprocal ST segment depression
Acute ST segment elevation
EKG Changes from Infarction
“T Wave Inversion”
Signs of Myocardial Injury
T wave inversion
• presence of ischemia
• May precede ST elevation
•Prominent in precordial chest leads
• Inversion in limb leads is pathologic
• T wave inversion can be caused by
other things than ischemia
EKG Changes from Infarction
“The Indeterminate Phase”
Signs of Myocardial Infarction
Pathologic Q-wave
•First indication of tissue death
•First few to several hours
•Q-wave ¼ size of QRS suggests
infarct
•Represent current or past events
•Determine timing through ST elevation
and T-wave inversion
Natural Progression of EKG in
Infarction
Over time:
•T-wave regains normal contour
•ST-segment returns to isometric line
•Q-wave remains as evidence of infarct
•Indicates presence of previous MI
*ST segment elevation
provides the strongest
evidence of early
recognition of AMI*
EKG Changes from Infarction
(cont.)
• All of the changes in the previous slides are: Indicative
Changes
• ST segment elevation is helpful in detecting an MI in its early
stages
• Hyperacute (Tall) T-waves alone are specific enough to
diagnose an MI
• T-wave inversion can occur with simple angina and is therefore
not specific
• Pathological Q-wave is the most accurate recognition of an MI
• Not in the first few hours
• ST segment elevation provides the strongest evidence for early
recognition of an MI
ECG Variants

Coronary Spasm:
“Printzmetals angina”
Injury pattern that resolves
w/ rest, NTG,O2 etc.

Early Repolarization:
elevated “J” point seen
best in V3,4. Key to Dx
pt’s are usually young &
asymptomatic

Pericarditis: ST elevation
usually global associated
w/ fever, pleuritic c/p.
ECG Variants due to Drugs or
Electrolytes Imbalances



Hypokalemia: lg U waves (
usually taller than T) seen best in
precordial leads. <2.7
Hyperkalemia:
–
Tall peaked T waves > 6.0
–
PR prolongs, QRS widens
–
P waves disappear > 8.0
Hypocalcemia:
–

Hypercalcemia:
–

Prolonged QT interval
Shortened QT interval
Digitalis effect:
–
–
–
–
ST depression- downsloping,
curved ST segments.
“scooping”, “sagging”, flat or
inverted T’s in lateral leads
PR prolonged
QT shortened
Bundle Branch Blocks
“Turn Signal Rule”
This is a simple method for differentiating right bundle branch block from
left bundle branch block. V1 will be the only lead you need to view
1. Locate the terminal (last) force of the QRS complex
2. Determine if it is pointing up or down.
3. Compare to the turn signal in your car:
» Up is for a right turn & RBBB
» Down is for a left turn and LBBB
Clinical significance:
Bundle branch is a significant complication of infarction. Since the left anterior descending artery is
the primary supplier of the bundle branches, BBB is considered a complication of anterior septal
infarcts.
When BBB is the result of MI, the incidence of pump failure is 65-70% and the in-hospital mortality
rate is 40%-60%. The BBB itself is not dangerous, but the high mortality rate is due to the extensive
amount of tissue death occurring when an infarct is serious enough to cause a BBB. Another
manifestation of BBB is in the form of AV Block. This is why infranodal AV blocks are more serious
and have wide QRS complexes.
Localizing the Area of
Infarction
•Indicative changes are not found in every lead
•Only present in leads looking at the infarct
•Indicative changes in two or more leads looking at the same
portion of the heart are anatomically contiguous leads
•Suspect AMI
•ST segment elevation in two or more leads that are not
contiguous
•AMI not the suspected cause
Recognition & Localization
•Recognizing infarct: Know which part of the heart each lead
looks at
•Localizing Infarct: Note which lead is displaying evidence and
which portions of heart they are looking at
Leads Displaying
Indicative Changes
II, III, aVF
Location of Infarct Site
Inferior
V1 & V2
Septal
V3 & V4
Anterior
V5, V6, I, and aVL
Lateral
*Simply knowing the changes to look for and which part
of the heart each lead looks at*
Anterior Wall MI
Anterior Wall infarct: Occlusion of the Left Anterior
Descending Artery (LAD)
•2mm ST segment elevation in two or more of leads V1-V4
•Reciprocal changes in leads II, III, aVF
•Lethal due to large myocardium involvement
Possible conduction defects:
Bundle Branch Block
2nd Degree Block Type II
CHB
Anterior Wall MI
Inferior Wall MI
Inferior Wall MI: Occlusion of Right Coronary Artery (RCA)
•At least 1mm ST segment elevation in leads II, III, aVF
•Reciprocal ST depression in leads I & aVL or precordial leads
Conduction defects:
•Sinus bradycardia
•Sinus arrest
•1st degree block
•Accelerated Idoventricular rhythm
Complications:
•Bradyarrhythmias – protective mechanism, 90% of blood supply for
SA & AV nodes from the RCA
•Hypotension – treated with fluids, consider right side involvement
Inferior Wall MI
Lateral Wall MI
Lateral Wall MI: results from occlusion of the Left
Circumflex Artery
•At least 1 mm ST segment elevation in leads I, aVL, V5 & V6
and /or 2 mm ST segment elevation in V5 & V6
•Reciprocal ST depression in V1
•Sometimes an extension of an Anterior or Inferior MI
•Conduction defects are rare
Anterior/Lateral Wall MI
Posterior Wall MI
Posterior Wall MI: Occlusion of the Right Coronary Artery
(RCA) or the Posterior Descending Artery
•No leads that look at the posterior wall
•Leads look at the infarct site from the opposite
side(backwards)
•ST depression in V1 & V2
•Tall R waves in V1 and/or V2
•Most often associated with Inferior MI
*Associated with dangerous conduction disturbances*
Posterior Wall MI
Right Ventricular MI
Right Ventricular MI: caused by proximal occlusion of the
Right Coronary Artery (RCA)
• Associated with Inferior Wall MI
• Can happen independently
• Standard 12-Lead does not assess right side of heart
• Infarction is significant
• Indicates large infarction
• Indicates involvement of both ventricles
• If the possibility of RVI exists a set of chest leads can be
applied to the right side of the chest
• V1-6R leads look at right ventricle
• Lead V4R most accurate
Right Ventricular MI
Septal Wall MI
Septal Wall MI: caused by septal perforation involving the
LAD or the Posterior Descending
•Most often in the setting of an Anterior MI
•Loss of R-wave in leads V1, V2 or V3
•May have ST segment elevation in V1 & V2
•No reciprocal changes
Overview of Infarcts
Location of
Infarct
Arterial
Supply
Indicative
Changes
Reciprocal
Changes
Anterior
LAD
V1-V4
II, III, aVF
Inferior
RCA
II, III, aVF
I, aVL
Lateral
Circumflex
I, aVL, V5, V6
V1
Posterior
Posterior
Descending
(RCA)
None
V1, V2
Septal
Septal Perforating Loss of R wave in None
(LAD)
V1, V2, or V3
Posterior
Descending (RCA
Overview of Infarcts
• Suspect infarction when there are indicative changes in at
least two anatomically contiguous leads
• Indicative changes in many leads suggests larger infarct
• With Inferior Wall MI suspect Right Ventricular Wall Infarct
• Signs of possible Right Ventricular Wall Infarct:
• Hypotension
• JVD
• Clear lung sounds
• Causes of ST segment depression include digitalis, ischemia
and reciprocal changes
• Suspect Posterior Wall Infarctions when an Inferior Wall
Infarction has ST depression in Leads V1-V3
Complications of Myocardial
Infarction
Chest Pain: Most common complication
• Treatment:
•Oxygen and ASA (162 to 325)mg
•NTG initially with Morphine if pain persists
• Usually very effective
Right Ventricular Wall Infarct:
• Reduces output of right ventricle decreasing left ventricular
filling (decreased preload)
• NTG and Morphine can worsen conditions
• Decrease in blood pressure will worsen area of injury
• Presence of Inferior Wall Infarction with no EKG or clinical
evidence of right side infarct does not merit any extra caution
when using NTG and Morphine
Complications of Myocardial
Infarction
AV Block Location: indicates electrical impulse from atrium
is blocked from depolarizing the ventricles
• Most common block is in the AV Node (nodal block)
• Second most common block is in the Bundle Branches
(infranodal)
• Infarct frequently produces AV Block due to increase in
parasympathetic tone
• Local ischemia around node can produce the block
• Less serious than block caused by tissue injury or death
• Blocks in AV node produce narrow QRS complex
• Bundle Branches produce wide complexes
Complications of Myocardial
Infarction
Determining the type of QRS presented with is a
useful tool in determining the location of the block
Coronary Supply
QR Width
Stability
Nodal Block
Right Coronary
Artery
Narrow
Generally Stable
Atropine Response Usually improves
Infranodal Block
Left Coronary Artery
Wide
Often Unstable
Often does not
respond
Complications of Myocardial
Infarction
Hypotension: A common treatment for hypotension
which is secondary to the infarct is to administer fluid
boluses and inotropic drugs (dopamine)
Hypotension in the setting of an inferior wall infarction is
most likely secondary to right ventricular involvement.
Although RV Infarcts may require significant boluses to
offset loss of preload, continuously monitor the patient for
signs and symptoms of developing left sided failure.
Hypotension in the setting of an anterior wall infarction
may not tolerate fluid boluses and may require a
dopamine infusion.
Complications of Myocardial
Infarction
Left Coronary Artery
Occlusions
Right Coronary Artery
Occlusions
Leads Showing
Indicative Changes
V1-V6, I, aVL
II, III, aVF, V4R-V6R
Localization
Septal, Anterior, Lateral,
Posterior
Inferior, Posterior, Right
Ventricular
Pain Control
NTG & Morphine as
appropriate
NTG & Morphine used
with caution if RVI
present
AV Block
Infrequent, usually wide
ORS, often unstable,
Atropine may be
ineffective, use standby
pacing
Frequent, usually
narrow QRS, Generally
stable, Atropine often
effective, May not
require treatment
Hypotension
200-250 cc fluid bolus,
inotropic medications
Vigorous fluid therapy if
RVI present, inotropic
medications
Clinical Pearls
• Suspect infarction when there are indicative changes in at
least two anatomically contiguous leads
• Indicative changes in a greater number of contiguous leads
suggests a more extensive infarction
• RV or Posterior infarcts should be considered in setting of
Inferior Wall MI
•RV: ST segment elevation in rV4
•Posterior: ST depression +/or Tall Rwave in V1 & V2
• Other clinical signs of RV Infarct may include:
• Hypotension and JVD in the setting of clear lung sounds
• Other causes of ST segment depression besides ischemia
include digitalis effects and ventricular hypertrophy
• Suspect Posterior Wall Infarctions when an Inferior Wall
Infarction has ST depression in Leads V1-V3
Questions