The 12-Lead EKG

Ben Taylor, PhD, PA-C

 Good Starting Place

• 42 year old male calls an ambulance with a

complaint of chest congestion and cough.
He has a history of a heart transplant for
ischemic cardiomyopathy 1 year ago. He
has been afebrile, but his chest hurts from
coughing.
• No tobacco, alcohol, or drugs.
 Auxillary (Heterotopic or ‘Piggyback’) Heart
Transplant
• Donor heart
• Native heart – S. rhythm, normal
– S. Tach, extreme RAD axis
– Features of old – Features of
anterolateral MI with Dextrocardia
deep Q-waves in leads I • Negative P in lead I
& V3-6
• Small QRS
complexes
decreasing in size
from V1 to V6

Lead I
Auxillary (Heterotopic or ‘Piggyback’) Heart
Transplant

Donor QRS complexes

Native QRS complexes

 Auxillary Heart Transplant

Negative P’s
deep Q-waves

Small QRS complexes V1 to V6

 Course Objective

• To systematically analyze the 12-lead ECG.

But First…
A Quick Review

A-fib

Junctional Tachycardia
PAC

PJC
Idioventricular Rhythm

Wandering Pacemaker
Normal Sinus Rhythm

Bigeminy
 Sinus Arrhythmia

Sinus Tachycardia
 Atrial Flutter

3rd Degree AV Block

 1st Degree AV Block

Ventricular Tachycardia
Accelerated Junctional Rhythm

Supraventricular Tachycardia
 Atrial Fibrillation (again)

2nd Degree AV Block type I (Wenchebach)

Sinus Rhythm with Unifocal PVC’s

Torsade de Pointes
Sinus Rhythm with Artifact

Junctional Escape Rhythm

So now we can begin our
Journey………
 Leads Used
Modern ECG's utilize 12 leads which are composed
of 6 limb leads and 6 precordial leads.

• Limb leads are: I, II, III, aVR, aVL, and aVF.

– (The lower case "a" in this notation refers to
"augmented" in the sense that the person who
developed the augmented leads discovered that he had
to augment or amplify the voltage in the EKG machine
to get a tracing that would be of similar magnitude as
leads I, II, and III.)
 Precordial leads

• V1, V2, V3, V4, V5, and V6.

• These measure the amplitude of cardiac
electrical current in an anterior-posterior
aspect with regard to the heart as opposed
to the chest (limb) leads which record in the
coronal plane.
 Steps in Interpreting The 12-Lead
1. Assess the rate (atrial and ventricular) and
regularity of the underlying rhythm.
a) Assess the usual intervals and widths: PR
interval, QRS width, QT interval.
b) Interpret the rhythm itself.
2. Determine the axis.
3. Grouped lead analysis
a) Look for signs of infarct vs. ischemia in all
grouped leads
4. Look for any other abnormality
 Grouped Lead Analysis

2. Lateral leads 3. Anterior leads

1. Inferior leads
 Assessing the EKG

Step II (Axis Step IV (Lateral lead Step V (Anterior

determination) analysis lead analysis)

Step III (Inferior lead

analysis)

Step I (Rhythm strip Step VI (find

analysis) everything else)
 Assessing the EKG Rhythm

Tip: the rhythm strip portion of the 12-lead ECG is a

good place to look at when trying to determine the
rhythm because the 12 leads only capture a few beats.

Atrial Rhythm?
fibrillation

Lead II

Rhythm
strip
 Assessing the EKG Rate
If you use the rhythm
strip portion of the
12-lead ECG the total
length of it is always
10 seconds long. So
you can count the
number of R waves in
the rhythm strip and
multiply by 6 to
determine the beats
per minute.
Rate?
14 (R waves) x 6 = 84 bpm
 Assessing the Axis
Axis refers to the mean QRS axis (or vector) during ventricular
depolarization. As you recall when the ventricles depolarize (in a normal
heart) the direction of current flows leftward and downward because most
of the ventricular mass is in the left ventricle. We like to know the QRS axis
because an abnormal axis can suggest disease such as pulmonary
hypertension from a pulmonary embolism.
 Assessing the Axis
The QRS axis is determined by overlying a circle, in the frontal plane.
By convention, the degrees of the circle are as shown.

The normal QRS axis lies between -30o and +90o.

A QRS axis that falls between -30o
-90o
and -90o is abnormal and called left -120o -60o
axis deviation.
-150o -30o
A QRS axis that falls between +90o
and +150o is abnormal and called 180o 0o
right axis deviation. 150o 30o
A QRS axis that falls between +150o 60o
120o 90 o
and -90o is abnormal and called
extreme right axis deviation.
 Assessing the Axis

• Causes of left axis deviation • Causes of right axis deviation

include:
– Left ventricular hypertrophy
– Inferior wall MI
– Left bundle branch block
– Left anterior fascicular block
-90o
include:
– Right ventricular hypertrophy
– Lateral wall MI
– Right bundle branch block
– Pulmonary hypertension

180o 0o

90o
 Assessing the Axis

We can quickly determine whether the QRS axis is normal by

looking at leads I and aVF.
If the QRS complex is overall positive in leads I and aVF, the QRS axis is
normal.

In this ECG what

leads have QRS
complexes that are
negative?
equivocal?
 Assessing the Axis
The thumb method
Always go with the positive thumb!!!!

Normal Axis Right Axis

Left Axis Extreme Right Axis

Normal, Right or Left Axis?

Normal
Normal, Right or Left Axis?

Right
Normal, Right or Left Axis?

Left
 Normal, Right or Left Axis?

Extreme Right
Normal, Right or Left Axis?

Left
 Assessing the Axis

Is the QRS axis normal in this ECG? No, there is left

axis deviation.

The QRS is
positive in I and
negative in aVF.
Take a Break
 Why Q-waves Form
• Region of myocardium dies  becomes….
– Electrically silent.
• As a result of this, the rest of the electrical
forces are directed away from this area of
infarction.
• Electrode overlying this area will record a
deep negative deflection – Q-wave.
Q wave = Necrosis (significant Q’s only)
• Significant Q wave is one millimeter (one small square)
wide, which is .04 sec. in duration…
• … or is a Q wave 1/3 the amplitude (or more) of the QRS
complex.
• Note those leads (omit AVR) where significant Q’s are
present
* A Q wave in lead III alone is not diagnostic of
infarction, even if it is otherwise “significant” in size and
width. Qs in III are ignored unless other abnormalities are
seen b/c they usually represent…..
• Old infarcts: significant Q waves (like infarct damage)
remain for a lifetime.
Normal vs. Abnormal Q-waves
EKG showing normal Qs in I,
AVL, V5 and V6
Q waves of old infarction in II, III,
and AVF
 Q Wave Summary

• Causes: Septal, Infarction

• Septal: I, AVL, V5-V6, occasionally
inferior leads
Significant: Q > 1/3 QRS, or
Q > 1 box wide and NOT in
lead III
Significant or Not?
Any Significant Q’s?

Yes in leads III & AVF only

 ST Elevation
• Signifies an acute process, ST segment returns to baseline with
time.
• ST elevation associated with significant Q waves indicates an
acute (or recent) infarct.
• ST depression (persistent) may represent “subendocardial
infarction,” which involves a small, shallow area just beneath
the endocardium lining the left ventricle. This is also a variety
of “non-Q wave infarction.
Causes of ST Elevation

• Infarction
Vasospastic angina
Pericarditis
Early repolarization
Is this ST Elevation?
 ST Depression Significance
• ST segment depression is considered
significant if the ST segment is at least two
boxes below baseline.
• With infarction, the location of the ischemia
is reflected in the leads in which the ST
depression occurs.
Common Causes of ST Segment Depression

• Ischemia
• "Strain" in LVH
• Digitalis effect
• Bundle branch block
• Hypokalemia/Hypomagnesemia
• Reciprocal ST elevation
• Any combination of the above
• The specific cause of ST segment depression in a given tracing
may be suggested by the appearance of the ST segment and T
wave itself. For example, “strain" (for LVH) is suggested by
asymmetric ST depression in lateral leads, especially if
voltage criteria are met.
• "RV strain" is suggested if the tracing depicted in the figure is
seen in right-sided leads in a patient with RVH.
• Ischemia is suggested by symmetric T wave inversion,
especially when seen in two or more leads of a group (i.e., in
II, III, and aVF).
 Digoxin Toxicity
• Digoxin ("Dig effect") may produce either ST
"scooping" or a "strain"-like pattern or no change
at all.
• Can be seen in levels greater than 2.5mg/ml
Dig Toxicity
 ST Segment
Depression

A = Normal ST segment
B = Junctional ST segment depression (frequently a normal variant -
physiological)
C = Upward-sloping ST segment depression
D = ST segment elevation suggestive of coronary vasospasm or AMI
injury pattern
E = Flattening of the ST segment with a sharp-angled ST-T wave junction
suggesting ischemia
F = Depression of the ST segment with U wave inversion
G = Sagging ST segment depression
H = Downward-sloping ST segment depression
What is your Dx?
If you think this is Ischemia or Dig
Toxicity

YOU’RE WRONG!!!! It’s early repolarization

 Characteristics of early
Repolarization
• Notching or slurring of the terminal portion of the
QRS wave
• Symmetric concordant T waves of large amplitude
• Relative temporal stability (when patients are
followed over time there will often be some variation
in the degree of ST segment elevation but generally
the change persists for years).
• Most commonly present in the precordial leads V2-5,
but often associated with pronounced ST segment
elevation in the limb leads II, III, & AvF
Early Repolarization
 R Wave Progression
• Normally the R wave becomes progressively
taller as one moves across the precordial leads.
• A number of conditions may be associated
with "poor" R wave progression, in which
the R wave in leads V1 through V3-V4 either
does not become bigger, or only increases very
slowly in size.
Causes of Poor R Wave Progression

LVH
RVH
Pulmonary disease (i.e., COPD, chronic asthma)
Anterior or anteroseptal infarction
Conduction defects (i.e., LBBB, LAHB)
Cardiomyopathy
Chest wall deformity
Normal variant
Lead misplacement
Good R-Wave Progression
Poor R-wave Progression
Just felt like throwing this in here

An education is a terrible thing to waste

 What is “Electrical Reciprocity”?
• Only two main areas of the heart that do this:
– Inferior and lateral ones
– Septal and posterior ones.
• A set of inferior ST elevations in II, III and AVF
can produce lateral ST depressions in I, AVL, V5
and V6. You’d think that this would mean lateral
ischemia, but no – it’s a reflection, bouncing
electrically across the heart from the inferior
injury, showing up in reverse.
Reciprocal Changes
Lateral MI, Inferior Reciprocity
Inferior MI, Lateral Reciprocity
What does ischemia look like on a
12-lead?

Not depressed

Or you could see

flipped T-waves

Way depressed
Anterior MI
Anterior Wall MI
Lateral MI
Lateral Wall MI
Inferior Infarct
Inferior Wall MI
Posterior Infarct
 Posterior Wall MI

Notice tall R wave in V1. Posterior wall infarcts are often

associated with inferior wall infarcts (Q waves in II, III and aVF).
Non Q-Wave Infarct
Now we search for everything else
of importance.
 Bundle Branch Blocks

• All forms of bundle branch block involve delays or

electrical blockages within the ventricles, they are all types
of intraventricular conduction deficits (IVCD). Bundle
branch blocks may also be categorized as either partial
(incomplete) or complete, depending on which patterns of
electrical activity are detected on an EKG.

• When the criteria for BBB are partially met (e.g. < 0.12
sec), this is termed “incomplete bundle branch block”
 Bundle Branch Block

• Widened QRS
complex
• RR’ configuration
in chest leads
 Risk factors and causes of BBB
• Degenerative effects of aging
• Hypertension
• Past heart attack that damaged the heart muscle
• Past viral infection
• Valvular heart disease, particularly calcific aortic stenosis
• One of several heart or lung conditions that could have
affected the ventricles (e.g., heart failure or chronic
obstructive pulmonary disease)
• Congenital condition
• Past injury to the chest
 Right bundle branch block
• When the right bundle branch is blocked, activation of the
right ventricle begins when electrical activity “spills over”
from the left ventricle. Depolarization of the right ventricle is
delayed.
• The QRS is prolonged (over 0.10 sec) in right bundle branch
block (RBBB). This extra length of the QRS is caused by late
activation of the right ventricle, which is then seen after the
left ventricle activity. Normally, right ventricle activity is not
seen, as it is overshadowed by the larger left ventricle.
• In RBBB, a typical RsR’ wave occurs in lead V1. Also, a wide
S wave is seen in leads I, V5, and V6, along with a broad R in
lead R. When RBBB occurs in a patient with old or new septal
infarction, the initial septal R wave may not be seen in lead
V1. Instead, a wide QR complex is seen.
Right Bundle Branch Block
Look for RR’ in leads V1 or V2
RBBB
 Left Bundle Branch Block
• LBBB usually indicates widespread cardiac disease. When
the left bundle is blocked, activation of the left ventricle
proceeds through the muscle tissue, resulting in a wide
(>.12 msec) QRS complex.
• In left bundle branch blockage (LBBB), the QRS usually
has the same general shape as the normal QRS, but is
much wider and may be notched or deformed. Voltage
(height of the QRS complex) may be higher.
• In LBBB, look for wide (possibly notched) R waves in I,
L, or V5-V6, or deep broad S waves in V1-V3. There is
left axis deviation. “Septal Q waves” sometimes seen in I,
L, and V5-V6 disappear in LBBB.
• T waves in LBBB are usually oriented opposite the largest
QRS deflection. That is, where large R waves are seen, T
waves will be inverted. ST segment depression may occur.
Left Bundle Branch Block

Look for RR’ in leads V5 or V6

LBBB
 Hemiblocks
• The two major branches of the left bundle may be
blocked individually. When only one branch is
blocked, this is called hemiblock — either
“anterior hemiblock” or “posterior hemiblock”
depending on whether the anterior or posterior
fascicles are involved.
• Hemiblocks are commonly due to loss of blood
supply to either the anterior or posterior division
of the Left Bundle Branch.
 Hemiblocks
• An occlusion of the Anterior Descending
Coronary Artery will produce an Anterior
Infarction, which often causes Anterior
Hemiblock.
• Left posterior hemiblock is less common
than left anterior hemiblock since the
bundle is much thicker and has a double
blood supply (left and right coronary
arteries).
ECG Criteria Diagnostic of Hemiblock
Syndromes
Anterior Hemiblock Posterior Hemiblock

Left axis deviation Right axis deviation

Q waves in lead I Q waves in lead III

Wide or deep S wave Wide or deep S wave

in lead III in lead I
A block of both the right and the left bundle branch is a complete AV block
 Bifascicular Block

LAD
RBBB
Q1, S3, So…..
LAHB + RBBB = Bifascicular Block
 Right Atrial Enlargement
• Right atrial enlargement (RAE) is
diagnosed by the presence of a P wave
2.5 millimeters or greater in height. The P
wave often has a sharp, peaked
appearance. This increased voltage is
caused by hypertrophy or acute strain of
right atrial tissue.
• The lead most likely to show the right
atrial enlargement is lead II.
• Causes of right atrial enlargement include
COPD, mitral stenosis, mitral
regurgitation, or pulmonary emboli.
Because RAE is so frequently seen in
chronic pulmonary disease, the peaked P
wave is often called “P pulmonale.”
 P-Pulmonale Pattern

P pulmonale in II, III, aVF P pulmonale in V1

Classic finding in Severe Right Atrial Enlargement (RAE)

Tall Peaked and Pointed P waves in the Pulmonary leads (II, III,
aVF). If the P wave looks "uncomfortable to sit on", think RAE!!!
SR, RAE, PJC
 Left Atrial Enlargement
• Dilation or hypertrophy of the left
atrium may increase the
DURATION of the P wave. (Recall
that right atrial enlargement causes
an increase in the HEIGHT or
amplitude of the P wave.) The P
wave is normally less than 0.11
msec (just under three small boxes).
• The long or abnormally shaped P
Left atrial enlargement often wave occurs because of delay in
occurs in mitral valve disease electrical activation of the enlarged
(either stenosis or insufficiency). left atrium, as electricity moves
Because of this association, a leftward from the SA node. A P
broad notched P wave is often
wave longer than 0.11 milliseconds
called “P mitrale.” In addition LAE
often occurs with any cause of left
is diagnostic of left atrial
ventricular hypertrophy.
enlargement (LAE).
 P-Mitrale Pattern
P mitrale in II, III, aVF P mitrale in V1

• Diagnosed by finding an m-shaped (notched) and widened P wave ( > 0.12 second) in a "mitral"
leads (I, II, aVL) and/or a deep negative component to the P in lead V1.
• Caused by conditions that increase either pressure or volume loading on the atria leading to
enlargement and/or hypertrophy.
– Longstanding hypertension
– Obstructive cardiomyopathy
– Aortic stenosis
– Aortic regurgitation
 Summary

• Atrial Enlargement Criteria

P > 2.5mm height = RAE
P > 0.11 sec or P notch > 1 box width
or P biphasic > 1 box square = LAE
 Right Ventricular Hypertrophy
• Right ventricular hypertrophy (RVH) increases the height of
the R wave in V1. An R wave in V1 that is greater than 7
boxes in height, or larger than the S wave, is suspicious for
RVH. Other findings are necessary to confirm the ECG
diagnosis.
– Other findings include right axis deviation, taller R waves
in the right precordial leads (V1-V3), and deeper S waves
in the left precordials (V4-V6). The T wave is inverted in
V1 (and often in V2).
• True posterior infarction may also cause a tall R wave in V1,
but the T wave is usually upright, and there is usually some
evidence of inferior infarction (ST-T changes or Qs in II, III,
and F).
• A large R wave in V1, when not accompanied by evidence of
infarction, nor by evidence of RVH (right axis, inverted T
wave in V1), may be benign “counter-clockwise rotation of the
heart.” This can be seen with abnormal chest shape.
RVH may occur with any process that raises the ejection work
in the right ventricle. This may be volume overload such as
atrial septal defect or tricuspid regurgitation, or may be pressure
overload such as pulmonary stenosis. Examples of pressure-
load causes of RVH include pulmonary stenosis or primary
pulmonary hypertension, pulmonary disease (COPD or
pulmonary emboli), large ventricular septal defect, or pulmonary
hypertension due to mitral valve disease.
SR, RAD, RVH with Strain
 Left Ventricular Hypertrophy

• Left ventricular hypertrophy is caused by increased loads

on the left ventricle. Examples are hypertension, aortic
stenosis or regurgitation, mitral regurgitation, or subaortic
stenosis.
• Left ventricular hypertrophy (LVH) may be difficult to
diagnose with certainty from the ECG. Different scoring
criteria have been recommended. One of the simplest uses
five criteria, with the certainty of diagnosis based on the
number of criteria present. If one is present, diagnose
“possible LVH”; if two, “probable LVH”; if three are
found, “definite LVH.”
 Multiple LVH Criteria
LVH Criteria #1:
Increased limb lead QRS voltage: R in lead I plus S in lead III greater
than 25 mm.
LVH Criteria #2:
Increased precordial QRS voltage: S in lead V1 plus R in either V5 or
V6 greater than 35 mm.
LVH Criteria #3:
Typical ST and T abnormalities: ST depression or T wave inversion
(or both) in the “lateral” leads (I, L, V4-V6)

LVH Criteria #4:

Large leftward voltage: R wave in lead AVL greater than 11 mm.
LVH Criteria #5:
Left atrial enlargement: Wide (greater than 0.11 msec) P wave. This
criterion is used IN SUPPORT of the diagnosis, not alone.
 Strain in Hypertrophy
• Strain is usually associated with ventricular
hypertrophy since a ventricle that is straining
against some kind of resistance (e.g. increased
resistance from a narrowed valve or from
hypertension) will become hypertrophied in its
attempt to compensate.
• The changes seen in the EKG are called secondary
repolorization abnormalities
• Ventricular strain depresses the ST segment, which
generally humps upward in the middle of the
segment.
 Strain

• Look for these

changes when
hypertrophy is present
to determine if there is
strain present:
– Downsloping ST
segment depression
– T-wave inversion
LVH with Strain
LVH with strain, possible LAE
 Summary

• RVH Criteria • LVH Criteria

R in V1 > 7 mm or > S 1) R-I + S-III >25 mm
wave 2) S-V1-2 + R-V5-6
T in V1 inverted >35 mm
Right axis deviation 3) ST-Ts in left leads
S waves in V5-V6 4) R-L >11 mm
5) LAE + other criteria
• Positive Criteria:
1=possible 2=probable
3=definite
 Diagnosis of Infarction with BBB
• This is difficult, but not necessarily
impossible. Look for ST-T wave changes
or new Q waves in left-sided leads (I, aVL,
V6) with LBBB.
• New onset of LBBB is typically
representative of an MI which you must
now R/O.
• Evidence of infarction (Q waves, ST-T
changes) is easier to see with RBBB.
 Diagnosis of LVH with BBB

• Suspect LVH with LBBB if there is LAA

and/or very deep S waves (>30 mm) in V1,
V2 or V3.
• LVH is probably present with RBBB if the
R in aVL is >12 and/or R in V5 or V6 is
>25.
 Pulmonary Embolism Criteria
• ECG findings noted during the acute phase of pulmonary
embolism can include any number of the following:
– “S1Q3T3” - prominent S in lead I, Q and inverted T in
lead III
– Right bundle branch block (RBBB), complete or
incomplete, often resolving after acute phase
– Right shift of QRS axis
– shift of transition zone from V4 to V5-6
– ST elevation in VI and aVR
– generalized low-amplitude QRS
– sinus tachycardia, atrial fibrillation/flutter, or right-sided
PAC/PVC
– T wave inversion in V1-4, often a late sign.
Pulmonary Embolism
S1

Inverted T Low voltage QRS throughout

Q3
 Pacemakers
pacemakers send electrical
impulses to one or more
chambers of the heart. These
signals make the heart
contract in a more regular
rhythm than the chamber
would otherwise. Pacemakers
are designed to treat cardiac
conditions that involve
bradycardia
What does a Pacemaker look like?

A pulse generator, which

contains both the battery
and the intelligent
circuits, can be very
small, as seen here. This
device can be connected
to a lead which makes
contact with either the
atrium or the ventricular
muscle.
 Pacer lead Wires
• Shown here are two leads. The
one on the top is a lead with a
"J" shape, which is used for
optimal positioning in the
atrium. It is "unipolar", and
therefore smaller, and is a
"tined" lead which makes
passive contact with the atrial
muscle.
• In contrast, the lead on the
bottom is larger because it is a
bipolar device which has more
wire within it. It has a small
screw at the end so that it can
be actively fixated to the
muscle.
 Dual Chamber Pacer
• Here, a pulse
generator is shown
which is connected to
two leads, for dual-
chamber pacing.
Pacemaker Insertion
Pacemaker Insertion
CXR after Insertion
External Surface of Chest
 Pacemaker Codes

Anti-
chambers chambers modes of programmable
tachycardia
paced sensed response functions
functions
1 2 3 4
5

V = Ventricle V = Ventricle T = Triggered R = Rate Modulated O = None

A = Atrium A = Atrium I = Inhibited C = Communicating P = Paced

D = Dual (A & D = Dual (A & D = Dual M=

S = Shocks
V) V) Triggered/Inhibited multiprogrammable

P = Simple
O = None O = None O = None D = Dual (P & S)
Programmable

--- --- --- O = None ---

 VVIMP
• Chamber paced - ventricle
• Chamber sensed - ventricle
• Response to sensing - Inhibits
• Program functions - multiprogrammability
• Antiarrhythmia functions - pacing
 Indications for Pacing
• Sick sinus Syndrome (most common) if
symptomatic
• 3rd degree AV block
• Recurrent tachycardias
• Chronotropic incompetence (inability to
increase the heart rate to match a level of
exercise)
• Long QT syndrome
 Atrial Pacemaker
• Sends out electrical signals to the upper part
of the heart which are passed down the
usual intrinsic conduction system to the
lower chamber.
– Only if the A-V node and the lower portions of
the electrical system are intact.
• Recommended so that the upper chambers
can initiate a heartbeat much like the natural
heartbeat.
 Atrial Pacing
• Atrial pacing is commonly seen in patients that have
damaged atrial pacing ability, but normal ventricular
conduction.
• Notice that the pacing spikes stimulate a P wave.
Atrial Pacemaker with 100% sensing & capture
 Ventricular Pacing

• Seen in patients with damaged ventricular ability

• Ventricularly paced rhythms generally have a
wide (> 0.12 secs) ORS complex following the
ventricular pacing spike.
Ventricular Pacing
Ventricular pacemaker with 100% sensing & capture
What is the Underlying
Rhythm?
 A-V Sequential Pacemaker
or
Dual Chamber Pacemaker
• A dual chamber pacer can sense and pace both
atrial and ventricular activity as programmed.
• Coordinates an electrical signal to the upper part
of the heart with a signal to the lower part of the
heart.
• When an individual requires a heartbeat similar
to a normal heartbeat, two wires are placed. One
wire detects the signal and/or stimulates the
upper chamber - atria. The other wire detects the
signal and/or stimulates the lower chamber -
ventricle.
 Standby Demand Pacemaker
• Ventricular inhibited
• Most commonly used type of pacemaker
• Sends out continuous, regular signals if
needed. Can turn itself off when the
individual’s heart sends out a competitive
beat.
• Fires when the pt’s own intrinsic HR falls
below a threshold level.
 Synchronous Demand Pacemaker
• Ventricular synchronous
• Sends out continuous, regular signals if needed. If
competitive heartbeats or electrical interference
occurs, responds up to maximum of 150 beats per
minute
• Recommended when individual will have contact
with special types of electrical machinery that can
lead to faster pacemaker activity.
• Upper pacemaker rate of 150 beats per minute
prevents unusually rapid heart rate during close
contact with machinery
 Pacemaker Abnormalities
-Failure to Capture-

• Characterized by pacing impulses (singly or in

groups) that are not followed by QRS
complexes and produce an irregular rhythm.
• Patient may or may not be symptomatic.
Pacemaker abnormalities
F-to-C
 Pacemaker Abnormalities
-Failure to Sense-
• Commonly caused by
a damaged sensing
lead that causes the
pacemaker to
misinterpret the
patient’s native rhythm
• Characterized by
inappropriate pacing
spikes that can occur
within ALL phases of
the cardiac cycle
Pacemaker Impulses
 Practice EKG 1

Infarct in the antereoseptal and anterior wall (Q waves in V2-V4 there is

also a probable inferior infarct (Q waves in II, III, and aVF)).
 Practice EKG 2

Ischemia across the entire anterior and lateral wall (T wave inversions in V2-V6, I
and aVL). Also note, the injury pattern in V2-3 of ST elevation, the prominent Q
waves in V2 and V3 show that some of the myocardium has also reached the
infarct stage.
 Practice EKG 3

Left anterior hemiblock (left axis deviation and Q1, S3).

Practice ECG 4

LAD, Poor R-wave progression

 Practice EKG 5

Left posterior hemiblock (right axis deviation and S1,Q3).

Practice EKG 6
What Do you See?
What Do you See?
What Do you See?
What Do you See?
This is what will happen…..

If you forget
what I taught
you