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 >
the preceding R-R

Putting the A&P with the EKG

Einthovens 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 isnt 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 Is

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 V25 with some ST
depression in aVF.

EKG after Acute Ischemia

This tracing was taken 30 minutes after the initial.

The patient was painfree 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 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
pts 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 Ts 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

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

Nodal Block
Right Coronary
Artery

Infranodal Block
Left Coronary Artery

QR Width
Stability

Narrow
Generally Stable

Wide
Often Unstable

Atropine Response Usually improves

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, Inferior, Posterior, Right

Posterior
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