MicroEKG Manual

What is an ECG?

The Machinery
The Standard Leads
The Augmented Leads
Limb Lead Vectors
The Chest Leads
The ECG Grid
Approach to the ECG

Parts of the ECG

The P Wave
The PR Interval
The QRS Complex
The ST Segment
The T Wave
The U Wave
The QT Interval

QRS Axis

Axis Deviation
Determining QRS Axis by Inspection
Vector Method for QRS Axis
Equiphasic Lead Method for QRS Axis

Ventricular Block

Right Bundle Branch Block

Left Bundle Branch Block
Hemiblocks

Chamber Enlargement

Right Atrial Enlargement

Left Atrial Enlargement
Right Ventricular Hypertrophy
Left Ventricular Hypertrophy

Diagnosis of Q Waves

ST and T Abnormalities

ST Depresssion
ST Elevation
T Wave Abnormality

Myocardial Infarction

Overview
Location of Infarction
Anterior Infarction
Lateral Infarction
Inferior Infarction
 Posterior Infarction
Subendocardial Infarction

Rhythm and Arrhythmia

Atrial Rhythms
Heart Block
Ventricular Rhythms
Ectopic Beats
Pacemaker Rhythm

What is an ECG?

The Machinery
The Standard Leads
The Augmented Leads
Limb Lead Vectors
The Chest Leads
The ECG Grid
Approach to the ECG
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The Machinery

An electrocardiogram is simply a measure of voltage changes in the body. Any large “electrical event” can be detected.
The electrically-active tissues in the body are the muscles and nerves. Small brief changes in voltage can be detected as
these tissues “fire” electrically. The heart is a muscle with well-coordinated electrical activity, so the electrical activity
within the heart can be easily be detected from the outside of the body.

The electrical changes that occur as the heart beats can be detected by
attaching two electrodes and measuring the voltage between them over
time. To do this, the ECG machine uses a roll of paper that moves at a
specific speed to represent passage of time, and has a stylus that moves up
or down with voltage to draw out the electrical events.

The heated stylus moves upward with positive voltage, downward with negative voltage, tracing out voltage versus
time on the moving heat-sensitive paper. To detect electrical activity moving in many different directions, it’s necessary
to have more than just one set of electrodes. (Electrical activity causes a voltage change only if it’s moving towards or
away from an electrode. If the electrical wave is moving at 90 degrees between the electrodes, it will not be detected.)

The Standard Leads

By attaching electrodes to the left arm, right arm, and either leg, we obtain the three “standard limb leads,” named I,
II, and III. Each of these leads measures voltage between two points on the body: left arm vs. right arm (Lead I), left
arm vs. foot (Lead II), and right arm vs. foot (Lead III).
 Lead I is obtained by measuring the voltage between the left arm and right arm.
The left arm is the positive pole. An electrical wave moving towards the left arm will
cause an upward deflection of the ECG machine stylus on the paper. Lead I is most
useful for seeing electrical activity moving in a horizontal direction.

Lead II connects the right arm to the leg, and therefore best sees electricity moving
down and leftward.

Lead III compares voltage in left arm and the leg, and will measure electricity moving
down and rightward. Lead II and Lead III are positive at the foot.

The Augmented Leads

Three additional limb leads can be obtained by mixing combinations of electrodes. These are leads R, L, and F.
To create these limb leads, two electrodes are connected together to create an “average” electrode, then connected
through the ECG machine to the remaining electrode.

Lead F is created by connecting the two arms together to create an “average”

electrode. To the ECG machine, this combination looks like a single electrode midway
between the two arms — directly in the center of the body above the heart. This
“average” electrode is connected through the ECG machine to the foot electrode.

This new ECG lead will detect electricity best if it’s moving straight up or down. The foot is the positive electrode, so a
downward motion of electricity will make the ECG stylus move upward on the paper. Lead F responds most strongly to
electrical activity that is moving straight up or down. Its “viewpoint” lies midway between lead II and lead III.
 Lead L is created by connecting the right arm and the leg together, then comparing
this “average” electrode to the left arm electrode. The left arm electrode is
positive, meaning that electricity moving to the left will cause an upward motion of
the ECG stylus.

Lead L sees electrical activity best if it’s traveling in a leftward and slightly upward direction. Lead L detects electrical
motion from a viewpoint midway between lead I and lead III. To see the direction in which lead L best detects
electricity, imagine a line between the right arm and foot. Find the halfway point, then draw an arrow from this halfway
point to the left hand. This arrow shows the “direction” of lead L; about 30 degrees above horizontal. Knowing the
direction of the various limb leads helps you localize pathology.

To create lead R, the left arm and the foot electrodes are connected together, then
the voltage of this “average” electrode is compared to the right arm lead. This gives
us a look at the electrical activity from a rightward and slightly upward direction.

Lead R is positive at the right arm electrode. This means that if electricity is moving in
a normal leftward direction, lead R will record a downward wave.

Lead R has a direction of 30 degrees above horizontal, aiming to the right. Because lead R “aims” in the opposite
direction from the other limb leads, its ECG waveforms will usually be “upside down” by comparison. In fact, lead R lies
exactly in the middle of the normal direction of electrical activity, but with the positive pole aiming away. This means
that every electrical wave in lead R should have a net negative direction, unless pathology is present.

Limb Lead Vectors

If the directions of all ECG limb leads are drawn out and superimposed on each other, the “EKG limb lead vector
diagram” is created. This diagram shows the orientation in which each limb lead best detects electrical activity. In the
vector diagram, the arrow indicates the direction in which that lead is positive (that is, motion in that direction will
cause an upward motion of the ECG stylus).

We assign the left side of lead I the value of zero degrees (no particular reason —
that’s just the way ECG folks have always done it). Clockwise from lead I is
positive, counterclockwise is negative.

Notice that each lead is 30 degrees apart. Lead L is pointing at negative 30

degrees. Lead II is oriented at plus 60 degrees, while Lead F’s direction is plus 90
degrees.
It’s important to know the orientation of the limb leads. For example, if the QRS wave is strongly downward (negative)
in lead I, you can conclude that electricity is traveling in an abnormally rightward direction, indicating a conduction
blockage in the heart. As another example, if you see signs of a heart attack in the leads that “look down” (lead III,
lead II, and lead F), you can conclude that the heart attack affects the bottom portion of the heart.

The Chest Leads

In addition to the six limb leads, a 12-lead ECG includes six “chest” leads. The chest leads “sample” the electrical
activity over small areas of the heart. The chest leads look at the heart’s electrical activity in a slightly off-horizontal
plane around the front of the chest. This detects problems that might not be obvious from the standard limb leads,
which measure electricity in a vertical plane.
The chest leads are often called V-leads. The electrode over the chest is the positive electode, while the limb electrodes
are all averaged together to form a general ground electrode.

The precordial (chest) leads start with V1, placed beneath the 4th rib to the right of the
sternum. Lead V2 is opposite V1 at the left side of the sternum. V3 is halfway to lead V4,
which is placed below rib 5 directly down from the middle of the clavicle. Lead V5 is
straight around the chest from V4, in line with the front of the armpit. V6 is directly
around from V5, straight down from the middle of the armpit.

The chest leads detect electricity moving in a front-to-back as well as side-to-side direction. Each lead responds to
electricity moving directly towards or away from it. These leads are useful for diagnosing problems on the front surface
of the heart, and for diagnosing ventricular hypertrophy.

The ECG Grid

The paper on which the ECG is drawn is divided up into 1 millimeter lines horizontally and vertically. The vertical lines
represent passage of time. Because the paper moves at a rate of 25 mm per second, each 1 mm line represents 0.04
seconds of time. Every fifth line is darkened to help with counting. The time between large boxes (darkened lines) is
0.2 seconds, and five large boxes equals one second.

The vertical direction represents the strength of electrical voltage. Positive

voltage moves the stylus up, negative voltage moves it downward. Each
millimeter vertically represents 0.1 millivolt. Ten vertical boxes is one
millivolt.

The horizontal direction represents passage of time.

Approach to the ECG

To avoid missing something important, it helps to have a “system.” A standard approach to every ECG may prevent an
unfortunate “miss” of a critical finding. Your standard plan should allow you to check every wave form and every
interval:

What is the rhythm? What is the rate?

Look for P waves. Are they all the same shape? Are there any inverted Ps other than in lead R? Does the PR interval
vary? Are there any non-conducted P waves? Is the P wave abnormally wide or high?
Check the PR interval. Is there first degree AV block? Is the PR abnormally short?

Look at the QRS complex in each lead. Is the QRS axis normal? Is the QRS width normal? Do the wave forms suggest
conduction block? Are there significant Q waves? Is the precordial R wave pattern normal? Are the QRS complexes too
small or too large?

Look at the ST segments. Is there an abnormality? Is the abnormality diagnostic of ischemia, infarction, or ventricular
strain?
Check the T waves. Is the shape normal? Are there inverted Ts in I, II, or V3-V6?

Look at the QT interval. Is it over half the R-R distance, or over 10 boxes in length?

Once you spot an abnormality, check for other findings that firm up the diagnosis. For example, when you spot a large
R in V1, you check for axis deviation, ST depression, and the orientation of the P wave in V1.

Parts of the ECG

The P Wave
The PR Interval
The QRS Complex
The ST Segment
The T Wave
The U Wave
The QT Interval
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The P Wave:

The P wave represents the spread of electrical

activity over the atrium. The normal depolarization
begins at the sinoatrial (SA) node near the top of the
atrium. Because of the top-to-bottom, right-to-left
path of the P wave, it’s normally largest in lead II.
The normal P wave is upright in all leads except R.

The P wave normally lasts less than 0.11 seconds (just less than three small boxes). An abnormally long P wave occurs
whenever it takes extra time for the electrical wave to reach the entire atrium. This occurs in left atrial enlargement.

The height of the P wave is normally less than 2.5 small boxes (less than 0.25 millivolts). An abnormally tall P wave is
seen when larger amounts of electricity are moving over the atrium. This usually indicates hypertrophy of the right
atrium. The P wave may be decreased in height by hyperkalemia.

The PR Interval:

Following the P wave is the PR segment. (NOTE: the PR segment and the PR interval are NOT the same thing.) The PR
segment is not routinely measured, but may be commented on if it is depressed or elevated. During the PR segment,
the electrical wave moves slowly through the atrioventricular (AV) node. This activity is not seen on the ECG.

The PR interval is the time from the beginning of the P wave until the beginning of the QRS complex. It is normally
between 0.12 and 0.2 seconds (three to five small boxes) in length.
The PR interval may be prolonged when conduction of the electrical wave through the AV node is slow. This may be
seen with degenerative disease of the node, or with digoxin, hyperkalemia, hypercalcemia, or hypothermia.

The PR interval may be unusually short when conduction is rapid. A mildly short PR interval may be seen with
hypokalemia or hypocalcemia. An artificially-short PR interval occurs when the QRS complex begins early, as happens
with an extra conducting bundle — Wolff-Parkinson-White Syndrome (WPW).

The QRS Complex:

The QRS complex represents activation of the ventricle. Special conducting bundles spread the wave of depolarization
rapidly over the ventricle.

The QRS complex is normally less than 0.10 seconds

in length — two and a half boxes. Lengthening of the
QRS indicates some blockage of the electrical action
in the conducting system. This may be due to
ischemia, necrosis of the conducting tissue,
electrolyte abnormality, or hypothermia.

If the first deflection of the QRS is downward, it’s called a Q wave. The Q wave represents activation of the ventricular
septum. The electricity spreads from right to left through the septum.

Q waves may be normal. For example in lead I, a Q less than 1/4 of the R height, and less than one box wide, is
considered normal. This is the early activation of the septum. This activation goes left — away from lead I — and is
therefore negative on the ECG. “Septal Qs” are normal in I, F, V5 and V6. Qs are also generally innocent in lead III and
lead V1 if no other abnormality is seen.

Q waves are “significant” if they are greater than 1 box in width (longer than 0.04 msec) OR are larger than 1/4 of the
R wave. Significant Q waves indicate either myocardial infarction or obstructive septal hypertrophy (IHSS).

The first upward deflection of the QRS is called the R wave. Most of the ventricle is activated during the R wave. The R
wave may be prolonged if the ventricle is enlarged, and may be abnormally high (indicating strong voltage) if the
ventricular muscle tissue is hypertrophied.

The S wave is any downward deflection following the R wave. Like the R wave, an abnormally large S wave may
indicate hypertrophy of the ventricle.

If a second upward deflection is seen, it’s called an R-prime wave. R-prime waves are never normal, but indicate a
problem in the ventricular conduction system.

QRS complexes may be described by naming the waves that form them. For example, a complex with an R, an S, and
an R’ is called an RSR’ complex.

The ST Segment:

The ST segment is the portion of the tracing falling between the QRS complex and the T wave. During this time, the
ventricle is contracting, but no electricity is flowing. The ST segment is therefore usually even with the baseline.
 The length of the ST segment shortens with
increasing heart rate. Abnormality of electrolytes may
also affect the ST segment length, however
measurement of the length of the ST segment alone
is usually not of any clinical use.

Upward or downward shifts in the ST segment are extremely important. Deviation of the ST segment from baseline can
indicate infarction or ischemia, pericarditis, electrolyte abnormality, or ventricular strain. ST segment elevation or
depression is generally measured at a point two boxes beyond the QRS complex.

The T wave:

The T wave represents the wave of repolarization, as the ventricle prepares to fire again. The T wave is normally
upright in leads I, II, and V3-V6. It is normally inverted in lead R. Ts are variable in the other leads (III, L, F, and V1-
V2).

T wave abnormalities may be seen with, or without ST segment abnormality. Tall T waves may be seen in hyperkalemia
or very early myocardial infarction. Flat T waves occur in many conditions. Inverted T waves may be seen in both
ischemia and infarction, late in pericarditis, ventricular hypertrophy, bundle branch block, and cerebral disease.

In young children, T waves may be inverted in the right precordial leads (V1 to V3). Occasionally, these T inversions
persist in young adults.

The U Wave:

A second wave following the T wave is called a U wave. Large U waves may be seen in electrolyte abnormality (such as
hypokalemia), or with drug effects.

The QT Interval:

The QT interval is the time from the beginning of the QRS complex until the end of the T wave. The “normal” QT length
varies with heart rate. Very fast rates shorten the QT length.
 At normal heart rates, QT length is abnormal if it’s
greater than 0.40 sec (10 boxes) for males and 0.44
sec (11 boxes) for females. Extreme QT
prolongations (greater than 0.60 sec — 15 small
boxes) predispose the patient to arrhythmias.

The QT interval may be prolonged with electrolyte abnormality, such as hypokalemia, hypocalcemia, or
hypomagnesemia. Myocardial ischemia may also prolong the QT interval.

QRS Axis

Axis Deviation
Determining QRS Axis by Inspection
Vector Method for QRS Axis
Equiphasic Lead Method for QRS Axis
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Axis Deviation:

The QRS axis is the “average” direction of electrical activity during ventricular depolarization. The QRS axis may shift
due to physical change in the position of the heart, chamber hypertrophy, or conduction block.

Normal QRS axis is from around -30 to degrees. More negative than -30 is
called left axis deviation. More positive than is called right axis deviation.

The average direction of electrical activity is the "QRS axis."

See the diagram: if the axis is in the direction labeled "II" the axis is degrees.

Right axis deviation is seen on the ECG when more electrical forces are moving to the right than normal. This is usually
due to hypertrophy of the right ventricle (RVH). Causes of right axis deviation include COPD, pulmonary emboli,
valvular disease, septal defects, and pulmonary hypertension.

An axis of is common in persons with emphysema. This so-called “vertical heart” reflects both the rotation of the heart
downward as the diaphragm position drops due to air trapping, and some degree of hypertrophy of the right ventricle.

Left axis deviation occurs when additional electrical forces move to the left (hypertrophy), or when the time required for
the electrical activity to move over the ventricle is prolonged (LBBB, left ventricular dilation).

Causes of left axis deviation include hypertension, aortic stenosis or regurgitation, subaortic stenosis, mitral
regurgitation, and left ventricular conduction defects.
The QRS axis may shift during the respiratory cycle if elevation of the diaphragm changes the physical position of the
heart. Beat-to-beat variation in QRS axis (an every-other-beat change in QRS shape) is called “electrical alternans.” This
is thought to be caused by the heart physically swinging back and forth in a pericardial effusion.

Determining QRS axis by inspection:

QRS Axis by Inspection

Method
The “inspection” method of determining axis requires that you lead I positive, lead III
check QRS orientation in specific leads. It is usually much faster positive = normal axis
than the vector method, and provides the same clinical lead I negative ( R positive)
information. = RIGHT axis
lead III negative, lead II
negative = LEFT axis

First check lead I. If the QRS is “positive” overall (comparing negative deflections to positive deflections), right axis
deviation is ruled out.

If the QRS in lead I is negative, right axis deviation is mild. Now check lead R. If the QRS is overall positive, right axis
deviation is definite.

Now check for left axis deviation by inspecting lead III. If the QRS is overall positive, left axis is ruled out.

If the QRS is negative in III, check lead II. If lead II also shows an overall negative QRS, left axis deviation is
diagnosed.

In this ECG, lead I is positive. Next we look at lead III and note it’s negative. We check lead II. Because lead III and
lead II are both negative, we diagnose left axis deviation by the “inspection method.”

Vector method for QRS axis:

Determining QRS axis by vector method is most easily done using lead F and lead I. These leads are convenient
because they are at right angles to each other.

First determine lead I’s QRS size and orientation by subtracting the S wave height from the R wave height. Then
determine lead F’s size in the same way.
 Plot out the overall QRS size on the line representing lead I. Positive is to
your right, negative to your left. Plot out the QRS size on the line
representing lead F. If F’s QRS is positive, draw downward. If negative,
draw up.

Draw lines perpendicular to the end points of your lines, to form a

rectangle. Draw a line from the centerpoint to the corner of your box. This
is the electrical vector. Its orientation represents the electrical axis

Remember that lead I is pointing to zero degrees, directly to your right (the patient’s left). Clockwise from lead I is
positive, counterclockwise is negative. In the diagram on the previous page, we would estimate the axis at minus 40
degrees.

Equiphasic lead method for QRS axis:

Another alternative for estimating QRS axis is the “equiphasic lead” method. Locate a lead that has the smallest total
QRS complex and/or is equiphasic. The QRS axis should be at 90 degrees to this lead.
Now look at the lead that (on the vector diagram) is 90 degrees from the equiphasic lead. If this lead’s QRS complex is
positive, the QRS axis is in the direction of that lead. If negative, the QRS axis is 180 degrees opposite.

In this ECG, lead III is most nearly equiphasic. The QRS axis will therefore be at 90 degrees to it. We would estimate
the axis at around plus 30 degrees.

Ventricular Block

Right Bundle Branch Block

Left Bundle Branch Block
Hemiblocks
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There are three conducting pathways from the AV node to the tissue of the ventricles: The “right bundle branch,” the
“left anterior fascicle,” and the “left posterior fascicle.” The combined left anterior and posterior fascicles are referred to
as the “left bundle.”

Bundle branch block occurs when electricity is not conducted down the one or more of the specialized conducting paths
in the ventricles. This may occur due to degeneration with age, or may be due to specific pathology such as myocardial
infarction. Bundle branch block widens the QRS, because electricity passes slower through muscle than through the
special conducting pathways. The form or shape of the QRS will change. Partial bundle block or hemiblock may be
diagnosed by a change in QRS axis or change in QRS shape, as the QRS is not widened in either partial block or
hemiblock.

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 0.1 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.

When the typical RsR’ wave is seen in V1 without widening of the QRS complex, this is called “right ventricular
conduction defect” rather than RBBB.

Right Bundle Block: Note the typical RsR’ wave in V1 with QRS width greater than 0.1 second.

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 Block: Wide QRS with broad R waves in I, L, and V5-V6. Typical ST and T abnormality.

Hemiblock:

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.

Left anterior fascicular block (anterior hemiblock, LAH) is diagnosed by NORMAL QRS duration with marked left axis
deviation, usually minus 60 degrees. S waves are larger than R’s in II, III, and F.

Left posterior fascicular block (posterior hemiblock, LPH) may be difficult to diagnose without prior ECGs. The QRS axis
shifts substantially rightward. An axis of over +120, with no evidence of RVH or anterior infarction, is presumed LPH.

Fascicular block can occur with RBBB. Most commonly, LAH may be accompanied by RBBB. On ECG, signs of RBBB are
accompanied by a leftward axis of -60 degrees.

When the QRS is prolonged without features of eather RBBB or LBBB, this is called “nonspecific intraventricular
conduction block.”

Chamber Enlargement

Right Atrial Enlargement

Left Atrial Enlargement
Right Ventricular Hypertrophy
Left Ventricular Hypertrophy
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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 increased voltage is best seen in the “inferior” leads —
those that see electrical activity moving from the top to bottom
— II, III, and F. 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.”

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 wave occurs because of delay in electrical activation of the enlarged left atrium, as
electricity moves leftward from the SA node. A P wave longer than 0.11 milliseconds is diagnostic of left atrial
enlargement (LAE).

Two other abnormalities indicate LAE. A “double hump” or

notched P wave is diagnostic of LAE if the peaks are one small
box or more apart. A biphasic P wave indicates left atrial
enlargement if the downward portion of the P wave is one box
or larger in both depth and length.

Left atrial enlargement often occurs in mitral valve disease (either stenosis or insufficiency). Because of this association,
a broad notched P wave is often called “P mitrale.” In addition LAE often occurs with any cause of left ventricular
hypertrophy.

Atrial Enlargement Criteria

P > 2.5 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.

RVH
Criteria
Other findings in RVH include right axis deviation, taller R waves in the right precordial
R in V1
leads (V1-V3), and deeper S waves in the left precordials (V4-V6). The T wave is
> 7 mm
inverted in V1 (and often in V2).
or > S
wave
 T in V1
inverted
Right
axis
deviation
S waves
in V5-V6

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.

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.”
The scoring criteria are discussed in detail on the next page. Please refer to the sample ECG.

Summary of LVH Criteria

1) R-I + S-III >25 mm
2) S-V1 + R-V5 >35 mm
3) ST-Ts in left leads
4) R-L >11 mm
5) LAE + other criteria

Positive Criteria: 1=possible 2=probable 3=definite

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 L 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.

Example of LVH

Diagnosis of Q waves

As you read the ECG, you must decide which Q waves indicate pathology, and which Qs are normal. For example in
lead I, a Q less than 1/4 of the R height, and less than one box wide, is considered normal.

“Normal” Qs indicate activation of the intraventricular septum. They will therefore appear in the leads that “look left” —
the rightward electrical activity across the septum will cause a negative deflection in these leads.

“Septal Qs” are normal in I, F, V5 and V6 (left or lateral leads). Small Qs are also generally innocent in lead III and lead
V1 if no other abnormality is seen.

EKG showing normal Qs in I, L, V5 and V6

Q waves are “significant” if they are greater than 1 box in width (longer than 0.04 msec) OR are larger than 1/4 of the
R wave. Significant Q waves indicate either myocardial infarction or obstructive septal hypertrophy (IHSS).
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.

In transmural myocardial infarction, significant Q waves (1 box wide or 1/4 the R) appear in the leads “looking at” the
area of infarction: II, III, and F for inferior infarction; I, L, and V5-V6 for lateral; and V2-V4 for anterior.

Q waves of old infarction in II, III, and F

Q waves that occur in the setting of LBBB or LVH are less reliable for diagnosis of myocardial infarction.

The presence of ST or T wave abnormality in the same lead(s) as “borderline” Qs makes these Qs suspicious for
infarction.
In idiopathic hypertrophic subaortic stenosis (IHSS) the Q waves tend to appear in the same leads in which normal
“septal” Qs are seen — because the pathology is thickening of the septum.

These “significant” Qs of IHSS are almost always accompanied by evidence of marked left ventricular hypertrophy.

Q Waves
Causes: Septal, Infarction, IHSS
Septal: I, L, V5-V6, occasionally inferior leads
Significant: Q > 1/4 R, or
Q > 1 box wide
and NOT in lead III
IHSS: increased “septal” Qs, evidence of LVH

ST and T Abnormalities

ST Depresssion
ST Elevation
T Wave Abnormality
Return to main MicroEKG manual index

ST segment depression

ST segment depression can be caused by ischemia, digitalis, rapid heart rate, and temperature or electrolyte
abnormality. It can also be a “reflected” or reciprocal ST elevation (showing an inverted view of what’s happening at
another place in the heart). The shape of the ST segment, and whether the abnormality is localized to leads looking at
one area of the heart, often allows the cause of ST depression to be diagnosed.

ST segment depression is considered significant if Causes of ST Depression

the ST segment is at least one box below baseline, Ischemia
as measured two boxes after the end of the QRS. As Hypothermia
with infarction, the location of the ischemia is Hypokalemia
reflected in the leads in which the ST depression Tachycardia
occurs. Subendocardial infarct
Reciprocal ST elevation
Ventricular Hypertrophy
Bundle branch block
Digitalis

Measure: 2 mm beyond QRS

Significant: 1 mm

Ischemia:

When ST segment depression is transient, it’s almost always due to acute myocardial ischemia. The ECG signs of
ischemia may come and go fairly quickly — over a matter of minutes.

ST segment depression is MOST specific for ischemia if the ST segment slopes down from the J point. Horizontal or flat
STs are also quite suspicous for ischemia. Upsloping ST depression is only about 60% accurate for diagnosing ischemia.

“J point” depression at the beginning of the QRS complex is not significant if the location of measurement (two boxes
past the QRS) finds the ST segment has risen back to the baseline.

Infarction:

ST depression can also be seen in infarction, typically in non Q-wave infarction, often called subendocardial infarction.
This type of infarct does not extend through the ventricular wall (non-transmural). Subendocardial infarctions involve
small areas of injured tissue, with larger areas of overlying ischemia. These infarctions may show ST segment
depression (rather than elevation) because of the larger areas of ischemia.

ST depression can also be seen as a “mirror” of what’s happening on the other side of the heart. For example, the
inferior leads may show ST depression as a reflection of what’s happening in the upper lateral side of the heart.

Ventricular hypertrophy:

Left ventricular hypertrophy or strain commonly causes ST segment depression, often with T wave inversions. These
changes are seen in the “lateral” leads — those that record activity over the left ventricle. In LVH, ST and T wave
abnormalities are commonly seen in leads I, L, and V4-V6.

Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2.

Ventricular conduction block:

Left bundle branch block produces ST depression and inverted T waves in leads I, L, and V5-V6. In general, the ST will
slope away from the direction of the QRS: a large wide R wave will have a down-sloping ST ending in an inverted T,
while a deep wide S wave will have an upsloping ST segment ending in an upright T.

Other causes of ST segment abnormality:

Patients on digitalis often show mild ST depression. This depression is usually less than 1 mm, and produces a
“scooped” appearance — the “Salvador Dali mustache” ST. These ST abnormalities are seen in multiple leads.

Hypothermia and severe hypokalemia routinely cause ST segment depression in multiple leads. Hypothermia will tend
to lengthen all ECG intervals, including the PR and QT, while hypokalemia will often lengthen the PR while shortening
the ST segment slightly.
ST segment depression is called “nonspecific ST abnormality” rather than “ST segment depression” if the ST segments
are less than 1 mm depressed and are accompanied by a normally-oriented T wave.
ST segment elevation

ST segment elevation is usually attributed to impending infarction, but can also be due to pericarditis or vasospastic
(variant) angina. In some healthy young adults, a form of ST elevation can be normal.

Causes of ST Elevation
Infarction
The height of the ST segment is measured at a Vasospastic angina
point 2 boxes after the end of the QRS complex. Pericarditis
ST segment elevation is considered significant if it Early repolarization
exceeds 1 mm in a limb lead or 2 mm in a
precordial lead. Measure: 2 mm beyond QRS
Significant: 1 mm limb lead
2 mm chest lead

Infarction:

In transmural infarction, ST segment elevation will be among the first manifestations. The ST segment elevation will be
seen in those leads involved in impending infarction.

ST segment elevation decreases as T wave inversion begins. ST segments may remain elevated when ventricular
aneurysm develops.

ST segment elevation that persists beyond three months following myocardial infarction suggests ventricular aneurysm.
ST elevation will be present in about 1/3 of ventricular aneurysms. When the patient with ventricular aneurism presents
with acute chest pain, a baseline ECG may help avoid misdiagnosis of impending infarction (and use of non-needed
thrombolytic drugs).

Vasospastic angina:

ST segment elevation can be seen in a severe type of ischemia called vasospastic or Prinzmetal’s angina. While exercise
angina involves the subendocardium, vasospastic angina causes severe transmural loss of blood flow. ST elevation
simply indicates injury, whether due to coronary thrombosis with impending infarction, or coronary spasm (Prinzmetal’s
angina). At this point, the injury is reversible.

Pericarditis:

Pericarditis, an inflammation of the space between the pericardial sack and outer surface of the heart, causes
widespread ST segment elevation. Physical damage and irritation of the heart’s surface produces a “current of injury” in
virtually all ECG leads.
Generalized ST segment elevation, unrelated to the distribution of any coronary artery, implies pericarditis. One must
be very cautious in diagnosing pericarditis from the ECG. For example, an inferolateral transmural infarction with pre-
existing junctional ST elevation in the anterior leads, could produce widespread ST elevation that could be confused
with pericarditis.

Later in the course of pericarditis, ST segment elevation resolves, without development of Q waves. After days to
months, ST elevation is replaced by widespread T wave inversions.

Early repolarization:

“Early repolarization” is a cause of ST elevation. This innocent condition typically occurs in young healthy males. The T
wave begins early, adding elevation to the ST segment.

Usually, early repolarization shows elevation of the J point (the junction between the end of the QRS and the ST
segment) and a concave upward curve towards the T wave. (“Concave upward” means the hollow portion of the curve
is on top.)
Early repolarization is usually seen in the anterior precordial leads of the ECG, but can be seen in limb leads to a lesser
degree.
Early repolarization cannot always be differentiated from myocardial infarction. In the chest pain patient, it’s safest to
assume ST elevation to be infarction until proven otherwise by reviewing a previous ECG or by obtaining serial ECGs.

T Wave Abnormalities

T wave abnormalities can provide added evidence to support clinical diagnosis. Except for hyperkalemia, T wave
abnormality alone is not diagnostic of any particular condition. The T wave must be considered along with QRS and ST
segment abnormalities. T waves will usually be abnormal in ventricular hypertrophy, left bundle branch block, chronic
pericarditis, and in electrolyte abnormality.

Tall, peaked T waves occur due to hyperkalemia. If the tall T waves are seen throughout the ECG, general
hyperkalemia is present. P waves will be small, PR interval short.

When typical tall, peaked T waves are seen only within a specific set of cardiac leads, it suggests impending infarction.
The tall Ts are due to potassium leak through damaged membranes in the area of the infarct.

T Wave Categories
Tall, peaked = hyperkalemia if generalized
infarction if localized
Inverted = evolving infarction
chronic pericarditis
conduction block
ventricular hypertrophy
acute cerebral disease
other cardiac disease
Flattened = nonspecific

In chronic pericarditis, T waves show wide-spread inversion, not corresponding to any coronary artery distribution.
General inversion of T waves can also be due to an evolving global subendocardial infarct.

Inverted T waves are seen during the evolution of myocardial infarction. The T inversion appears in the leads “looking
at” the infarcted area. Several hours after an infarct, T waves begin to invert. T wave inversion may persist for months.

Left ventricular hypertrophy or strain commonly causes T wave inversion. In “strain” pattern, the ST segment slopes
down to an inverted T in the leads “looking at” the affected ventricle.

Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2.
The T wave will be inverted over right heart leads showing evidence of hypertrophy and strain.

Left bundle branch block can cause ST depression and inverted T waves in leads I, L, and V5-V6. The ST depression is
usually not great. The T wave tends to be oriented opposite the QRS in LBBB.

Flat T waves can be seen in many conditions, including ischemia, cardiac scar, evolving infarction, and electrolyte
abnormality (such as hypokalemia).

In acute cerebral disease, such as intracranial hemorrhage, elongated or bizzare T waves may be seen. These Ts are
often biphasic or deeply and sharply inverted. The QT interval is often dramatically lengthened (0.5 to 0.7 seconds).

Myocardial Infarction

Overview
Location of Infarction
Anterior Infarction
Lateral Infarction
Inferior Infarction
 Posterior Infarction
Subendocardial Infarction
Return to main MicroEKG manual index

Overview

Infarction is diagnosed by examining the QRS complexes, ST segments, and T waves. Combinations of abnormalities
are usually required to make the diagnosis. Changes over time may also be required to firmly diagnose infarction.

The ECG signs of impending, evolving, and completed infarction follow a course from peaked T waves to elevated ST
segments, to development of Q waves, to development of T wave inversion and resolution of ST segment elevation.
The abnormalities you should look for are: “significant” Q waves, loss of precordial R height, ST elevation in contiguous
leads, and T wave peaking or inversion. Any combination of these abnormalities can be present during the evolution of
infarction.

Tall, peaked T waves in the area of ischemia may be the first sign of tissue injury. These tall T waves are identical to
those seen in hyperkalemia, but are localized to the leads “looking at” the area of injury. These waves are probably due
to potassium leaking through damaged membranes.

Anterior infarction shows ST changes in the anterior precordial leads.

ST segment elevation is seen in early transmural infarction. ST elevation is reversible if blood flow through the occluded
coronary artery is restored. The ST elevation is seen in the leads directed towards the area of injury. Transmural
infarcts (where the entire thickness of the heart muscle is affected) are usually caused by coronary artery thrombosis.

ST segment depression may also be seen in infarction. It may be: 1) primary ST depression due to a large area of
relative ischemia surrounding a small area that is infarcting, such as in subendocardial infarction, or 2) “reciprocal”
changes, where ST depression is seen in leads “opposite” those that show ST elevation. For example, anterior infarction
can cause ST depression in the inferior leads.
 Recent anterior infarction shows Q waves, inversion of the T wave.

Old anterior infarct shows normalization of the ST segment and T waves, but loss of R wave in V2-V3, Q in V4.

The last sign of infarction to occur is the Q wave. Q waves appear only with larger, transmural infarctions. Most often,
the Q waves become a permanent reminder of the infarct. They allow diagnosis of a previous infarct years after the
event.
After infarction is complete, the ST segment elevation resolves and the T waves become inverted. This sequence of
events “firms up” the clinical diagnosis of infarction.

Clinical diagnosis of infarction uses the ECG as a tool to assist in the diagnosis. The ECG does not “make” the diagnosis.
The ECG of a patient with acute anterior infarction may appear exactly the same as that of a patient with an anterior
ventricular aneurism.

The usual criteria for clinical diagnosis of infarction (sufficient to warrant use of thrombolytic drugs) are: 1) typical,
significant ST segment elevation in two or more contiguous leads, and 2) typical chest pain of over 15 minutes
duration, not responsive to nitroglycerin.

Location of Infarction

ECG leads can be divided into zones. Changes diagnostic of infarction within a “zone” of leads indicate infarction in the
geographic area of the heart forming that zone of ECG leads. The four identifiable areas for infarction are inferior,
lateral, anterior, and posterior, or a combination of these areas. Infarcts may also be classified as transmural (involving
the entire wall of the heart) or subendocardial (affecting only the most sensitive inner area of heart muscle).
Localization of ECG Pathology
Inferior: Abnormalities that appear in leads II, III, and F (called the
inferior leads) indicate pathology on the inferior or diaphragmatic surface of
the heart.
Lateral: Leads I, F, and V5-V6 are called lateral leads. Abnormality in these
leads indicates pathology on the lateral, upper surface of the heart.
Anterior: Anterior pathology is seen in leads V1-V4, and often in lead I.
Posterior: Problems on the posterior surface of the heart are difficult to
diagnose using the standard 12 ECG leads. The pathology may be seen
“reflected” through to V1 and V2.
Combination: Abnormalities may not be limited to one of the four areas
above. Inferolateral damage will show up in a combination of the inferior
and lateral leads. Anterolateral damage will be seen in a both the anterior
and the lateral leads.

Anterior infarction:

Infarction of the anterior wall is caused by occlusion of the left anterior descending coronary artery. Signs of infarction
will usually be seen in lead I and V2-V4, and often in V1.

Anterior infarction may be diagnosed if significant Qs (or QS complexes) are seen in lead I and any of V2-V6, or if a
significant Q is seen in lead L when at least 3 mm of R wave is present.

Also highly suspicious are significant Qs in V2-V6. In the anterior leads, even a small Q should be considered significant
when the Q is followed by an R wave and larger S wave. “Non-pathologic” Q waves are seen in V2-V3 only if the heart
is rotated counterclockwise (these leads would then correspond to V5 and V6, where small Qs are normal).

Acute anterior infarction

“Poor R wave progression” can suggest the possibility of anterior MI, but is not diagnostic. Normally, R waves become
larger as the ECG moves from V1 to V4. An actual decrease in R wave height from one anterior precordial lead (V2
through V4) to the next is highly specific for infarction.

Lateral infarction:

Lateral wall infarction can result from occlusion of the left circumflex coronary artery, or from a lateral branch of the left
anterior descending artery. ECG changes are seen in leads I and L, V5-V6.
 Acute lateral wall infarction

Anterolateral infarction involves portions of the anterior and the lateral walls of the heart. Lateral branches of the left
anterior descending artery are at fault. ECG evidence of anterolateral infarction is seen in the more lateral anterior
precordials, as well as the lateral leads. Leads I, L, and V4-V6 will be involved, with some degree of involvement of V3
and possibly V2.

Inferior infarction:

Occlusion of a dominant right coronary artery produces inferior infarction, with ECG evidence seen in leads II, III, and
F. The inferior portion of the heart is supplied by the right coronary artery in most persons, but can also be serviced by
the left circumflex artery, or by both.

Recent inferior infarction

When “significant” Q waves are seen in all three inferior leads, this is highly specific for MI. (These Qs must be either
0.4 msec, deeper than 5 mm, or the Q must be over 1/4 the size of the R wave.) If Qs are seen in only II or F, but are
both wider than 0.4 msec (1 box) and larger than 1/4 the R size, this is “moderately specific” for inferior infarction.

If the inferior portion of the heart is served by the left cirumflex artery, inferior infarction may be accompanied by
lateral infarction, called inferolateral infarction. ECG signs are seen in both inferior leads (II, III, F) and lateral leads (I,
L, and V5-V6).

Posterior infarction:

Occlusion of the right coronary artery may also produce posterior infarction — with or without inferior infarction. True
posterior infarction is difficult to diagnose.

True posterior infarction may produce changes only in lead V1 and V2. The ECG changes of posterior infarction are
“reciprocal” changes, that is, they are seen “backwards” on the front of the heart in lead V1. Qs become big R’s, ST
elevation is seen as depression, T inversion is seen as an upright T. Lead V1 and V2 have large R waves, which are
“reflected Q waves” from the back of the heart. The ST segment depression is “reciprocal” or “reflected” ST elevation
from the back of the heart. T waves will become upright.

In true posterior infarction, no abnormality is seen in the limb leads. However, posterior infarction is usually
accompanied by infarction of another area, such as the inferior wall.

Subendocardial infarction:

One final location for myocardial infarction is “global subendocardial.” This infarction occurs when a person with diffuse
coronary disease has an episode of hypotension and/or extraordinary myocardial oxygen demand.

The global subendocardial infarction involves widespread areas of the endocardium, with evidence of infarction showing
up in anterior, inferior, and lateral leads. Widespread subendocardial infarction may be difficult to differentiate from
pericarditis on initial ECG.

Rhythm and Arrhythmia

Atrial Rhythms
Heart Block
Ventricular Rhythms
Ectopic Beats
Pacemaker Rhythm
Return to main MicroEKG manual index

Sinus rhythm:

Normal rhythm, called sinus rhythm, is paced from the sinoatrial (SA) node. The heart rate for normal sinus rhythm is
from 60 to 100 beats per minute. Sinus rhythm faster than 100 beats per minute is called sinus tachycardia; slower
than 60 is called sinus bradycardia. Sinus rhythms show a normally oriented P wave before each QRS complex.

Ectopic atrial pacemaker:

The normal P wave should be upright in all leads except R. If the QRS is preceded by an abnormally-oriented P wave
(often with a shortened PR interval) this indicates an ectopic atrial pacemaker. The heart is being paced by atrial tissue
somewhere outside the sinus node. The ectopic P wave may have an odd shape.

Many different P wave shapes suggest multifocal ectopic atrial pacing.

Multifocal atrial rhythm:

If three or more different P wave shapes are seen, multifocal atrial pacing is diagnosed. This condition is often seen in
chronic lung disease with right atrial enlargement. Several atrial locations are competing for control of the rhythm,
resulting in P waves of differing shape and/or PR interval. Because the P waves occur at differing times, the rhythm
tends to be irregular. If the rate is over 100, it’s called multifocal atrial tachycardia.

Paroxysmal supraventricular tachycardia (PSVT or PAT):

In this condition, clock-regular tachycardia occurs due to a circular motion of electricity within the atrioventricular (AV)
node. QRS complexes are usually narrow, but if conduction blockage is present downstream from the AV node, the QRS
may be wide, causing confusion with ventricular tachycardia. If electricity exits the node into the atrium after
ventricular contraction, “retrograde” inverted P waves may be seen after the QRS complexes, but this is uncommon.

PSVT

Atrial flutter:

Atrial flutter is a fairly organized back-and-forth motion of electricity within the atria. The rate of atrial depolarization is
typically 300 beats per minute. Usually every other atrial beat is blocked in the AV node, resulting in a typical
ventricular rate of 150. With increasing AV block, the rate may slow to 50, 75, or 100 (if the rate is regular, it will be
some fraction of 300). Occasionally, such as in WPW syndrome, atrial beats will be conducted 1:1, resulting in a
ventricular rate of 300. When the ventricular rate is slowed enough to see the atrial activity, a typical “sawtooth”
baseline is seen, with the peaks appearing 5 mm apart.

Atrial fibrillation:

Atrial fibrillation is random electrical activity in the atrium, with ventricular beats occurring irregularly. Ventricular
depolarization occurs whenever an electrical impulse arrives at the AV node when it’s ready to conduct. QRS complexes
may be wide when conduction block is present. The rate in atrial fibrillation may be very rapid, or slow, depending on
the conductivity of the AV node.

Atrial fibrillation

Pre-excitation syndrome:

Wolff-Parkinson-White (WPW) syndome occurs when a band of conducting tissue bypasses the normal AV node path.
This results in early activation of a portion of the ventricle. The PR interval will be abnormally shortened, with an
abnormally-shaped wide QRS following. The QRS usually has a typical “delta wave” (an early slow upstroke of the R
wave prior to a fairly normal-looking QRS).
WPW syndrome often results in paroxysmal supraventricular tachycardia. Other atrial arrhythmias may cause a severe
tachycardia, as the extra conducting pathway delivers every atrial depolarization to the ventricle. For example, atrial
flutter may result in a ventricular rate of 300 due to 1:1 conduction. Atrial fibrillation results in a chaotic tachycardia.
WPW syndrome is important to recognize, because the treatment may differ from “ordinary” PSVT.

Junctional rhythm:

This rhythm originates in the AV conducting system. A regular, narrow QRS complex is seen, often at a rate of around
75, without normal P waves preceding it. Often an inverted P wave can be seen just after the QRS complex.
Occasionally, the inverted P wave is seen at the beginning of the QRS complex, coupled too closely to be an ectopic
atrial pacemaker. Junctional rhythm with atrial fibrillation and complete heart block usually indicates digoxin toxicity.

First degree AV block:

This is an atrial-paced rhythm with a prolonged PR interval, but with conduction of every atrial beat to the ventricle.
The PR interval exceeds 0.2 seconds.

Second degree AV block:

Second degree atrioventricular block is an atrial-paced rhythm where some, but not all, of the atrial beats are blocked
from the ventricle. This type of block is further divided into Type I and Type II.

Type I second-degree AV block is often called “Wenckebach” block. This block occurs high in the AV node, and is
usually caused by acute, reversible conditions. It is usually treatable and rarely goes on to complete heart block. In
Wenckebach block, the AV node “fatigues” with each beat, causing a lengthening PR interval. Finally, a beat is blocked.
Then the process begins again.

Type I or Wenckebach AV block -- slowing of conduction through the node

In Wenckebach block, the interval between QRS complexes actually shortens slightly until the dropped beat. This is
because, while the AV delay becomes greater with each beat, the INCREASE in the AV delay is greatest with the first
beat. The amount of extra delay added to the PR with each beat decreases after the first beat. This makes the R-R
interval shorten until a beat is blocked.

Type II second-degree AV block is a blockage below the AV node. Often only one fascicle is conducting — that is, the
conducted beats may show LBBB or RBBB with hemiblock — but is conducting only intermittently. If the block is above
the junction between the left and right bundles, the QRS may appear normal, but this is rare. This type of AV block
often progresses to complete (third degree) heart block.

Type II second-degree block -- damage to the conducting bundles

Type II block can be diagnosed if two consecutive conducted beats have the same PR interval.

If the rhythm is 2:1 (i.e., every other P wave is blocked) it may be difficult to diagnose type I versus type II. The
benign type I is more common. If the PR interval is prolonged and no bundle branch block is present, assume type I. If
the PR interval is normal and there is a bundle block, assume type II. If the ECG shows both long PR and bundle block,
the mechanism of second-degree AV block can’t be diagnosed.

Complete AV block:

Complete AV block is also called third-degree heart block. No atrial impulses reach the ventricles. The atrial P waves
bear no relation to what’s happening in the ventricles. The ventricles will usually develop an “escape rhythm.” If the
lower AV node assumes the role of pacemaker, narrow regular QRS complexes may be seen. This is often called a
“nodal escape rhythm.” If the ventricular muscle becomes the pacer, a wide-QRS ventricular escape rhythm will
develop, at a rate of around 30.

Pseudo-AV block:

Non-conducted extra beats originating the AV node may make the node refractory to the next electrical wave, causing a
single-beat AV block. This may be an isolated prolonged PR interval, or a dropped beat. If these “occult PVCs” occur
regularly, they can be differentiated from Type I second-degree block by the absence of lengthening PR prior to the
dropped beat.

Ventricular tachycardia:

Ventricular tachycardia is a regular, wide-complex tachycardia originating within the ventricles. It may be caused by an
irritable area in the ventricle acting as a rapid pacemaker, or may originate via a circular motion of electricity in an area
of damaged myocardium.

Ventricular tachycardia

If atrial activity continues during the episode of V-tach, P waves may be seen deforming the ventricular complexes.
Occasionally, an atrial depolarization may be conducted, resulting in a narrower QRS complex. This narrow QRS may
resemble the patient’s standard QRS complex, or may be a hybrid between the V-tach QRS and the normal QRS, called
a fusion beat. Either of these findings confirms that the tachycardia is V-tach rather than an aberrantly conducted
supraventricular tachycardia.

V-tach that changes orientation (changes QRS axis) regularly over a period of many beats is called Torsades de pointes.
This type of tachycardia may be caused by hypomagnesemia (among other etiologies), and is important to recognize
because its treatment may differ from standard ventricular tachycardia.

Torsades de pointes -- V-tach with changing axis

Ventricular fibrillation:

Ventricular fibrillation is chaotic irregular electrical activity within the ventricles. No QRS complexes are seen. V-fib is
referred to as “course fibrillation” if the waves of electricity cause large deviations of the ECG baseline, and as “fine
fibrillation” if the electrical waves are of low amplitude.

Ventricular fibrillation

Premature Beats

Premature beats (PVCs, extrasystoles) may be atrial, nodal, or ventricular in origin. The cause of premature beats can
often be surmised from careful attention to preceding atrial activity, length of preceding R-R interval, length of the
following R-R interval, and the QRS shape.
Lead II and lead V1 are most useful for differentiating premature beats, because the P waves are most obvious in II
and the QRS shape is most helpful in V1.

Atrial premature beats:

Premature beats preceded by a P wave (with a reasonable PR interval) are atrial premature beats. The P wave often
has a different shape or size compared to the patient’s normal P’s. The pause after the QRS before the next beat is
about the same as for the normal sinus R-R interval because the ectopic P wave will “reset” the sinus node.

Premature beat triggered by ectopic P wave

AV node premature beats:

Premature beats that cause an inverted P wave to appear during the ST or T wave are originating in the AV node. The
QRS is usually narrow. When the QRS is wide, the extra beat may be either an aberrantly-conducted nodal beat, or a
ventricular extrasystole with retrograde conduction through the AV node. AV node premature beats may also be seen
with an inverted P wave immediately in front of the QRS with an impossibly-short PR interval.

Ventricular premature beats:

Ventricular premature beats rarely disturb the underlying sinus rhythm. There will usually be a full “compensatory”
pause after the extra beat: the distance from the previous normal beat to the normal beat following the PVC is the
same as two normal R-R intervals. After the PVC, the sinus beat is blocked, and the pause occurs as the ventricle
“waits” for the next sinus beat. With slower heart rates, a very early PVC may appear “inserted” between two normal
sinus beats with normal R-R interval. PVCs usually have a wide QRS, often oriented all in one direction
(monophasic). A PVC may have a normal-width QRS complex if it originates in the conducting system.
 Premature ventricular beats in bigeminy pattern

PVCs that occur at a regular interval, completely independent of conducted complexes, are called parasystole.

PVCs versus aberrant conduction:

Beats originating in the atrium may have a wide QRS complex due to abnormal (aberrant) conduction. Wide-QRS
ectopic beats can be attributed to atrial extrasystoles if 1) an ectropic P wave is identified, 2) the beat occurs
immediately following two normal beats separated by a longer R-R interval and has a “bundle-branch block” type QRS
form.

In lead V1, most PVCs will tend to have a “big-R, smaller R” form. PVCs tend to be monophasic: the QRS complex is
oriented all in one direction.

A “small-R, bigger-R” QRS form, or an rSR-prime, is usually aberrant conduction of a supraventricular beat. The initial
portion of the QRS is usually identical to the normally-conducted beats.

An irregular-spaced, wide-complex tachycardia is almost always supraventricular in origin. Also, a run of wide-complex
tachycardia is presumed to be atrial in origin if it’s immediately preceded by an ectopic P wave.

Recognizing Aberrant Conduction

Preceding P wave
Initial portion of QRS identical to conducted beats
Right bundle block pattern
Follows after long R-R interval
No compensatory pause

Recognizing PVCs
No preceding atrial activity
Monophasic QRS
Big-R, little-R pattern
Compensatory pause

Pacemaker Function

Pacemaker spikes may be seen on the ECG. If possible, determine: Does the pacemaker SENSE? Does the pacemaker
CAPTURE?

We will consider the standard “VVI” pacemaker: it paces the ventricle (V), senses spontaneous depolarization of the
ventricle (second V), and is inhibited (I) from firing when it detects firing of the ventricle faster than a pre-set
threshhold.

To determine sensing, find an area on the tracing where the heart rate is higher than the threshhold. See if the
pacemaker turns off. Pacer spikes should disappear.

Find an area where the rate drops to the threshhold. To determine capture, see if each pacer spike is followed by a
ventricular contraction. This linkage of spike to QRS is called “capture.”
 Paced rhythm with single failure to capture

If the patient’s own heart rate remains above the threshhold for pacing, you must “induce” the pacemaker to determine
whether the pacer is functioning. A magnet (made specifically for this purpose) placed over the pacemaker turns
sensing off. The pacemaker will fire as though the patient’s rhythm is too slow. When a spike occurs after the
“refractory period” it should capture the ventricle.

The “magnet rate” will often be different from the pacing rate. A slowing magnet rate may indicate the need for
pacemaker battery replacement.

All material referenced through this menu is excerpted from copyrighted works by Bruce Argyle, MD. You are welcome
to use selected portions, as long as appropriate credit is given. The credit for the text referenced through this menu is:

Argyle, B., MicroEKG Computer Program Manual.

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