Primer

Basic surface electrocardiogram interpretation for the

pharmacist
Philip L. Mar, MD, PharmD, Division
of Cardiology, Department of Medicine, Purpose. The electrocardiogram (ECG) is an invaluable tool for clinicians
Saint Louis University School of
Medicine, Saint Louis, MO, USA
that provides important information about a patient’s heart. As clinical
pharmacists play an ever-increasing role in cardiovascular care, ECG in-
Joseph S. Van Tuyl, PharmD, Saint

Downloaded from https://academic.oup.com/ajhp/article/78/10/850/6145841 by University of Cambridge user on 27 May 2021

Louis College of Pharmacy, Saint Louis,
MO, USA
Michael J. Lim, MD, Division of
Cardiology, Department of Medicine,
Saint Louis University, Saint Louis, MO,
USA
terpretation is an important skill with which to become familiar.
Summary. The ECG provides information on both electrical and biomech-
anical aspects of the heart. Electrical information such as the rhythm, rate,
and axis of the electrical activity can all be provided by the ECG. Biomech-
anical information about the heart, such as the presence of ventricular
hypertrophy and repolarization changes that may be associated with is-
chemia or myocardial injury, can also easily be gleaned from the ECG. Fur-
thermore, the ECG plays a central role in both the diagnosis and treatment
of common clinical conditions such as atrial fibrillation, ischemic heart dis-
ease, and QT interval prolongation.

Conclusion. The ECG is one of the most commonly performed diagnostic

tests, and clinicians should become familiar with its basic interpretation.

Keywords: arrhythmia, cardiology, electrocardiogram

Am J Health-Syst Pharm. 2021;78:850-861

Address correspondence to Dr. Mar
(Philip.mar@slu.edu).
© American Society of Health-System
Pharmacists 2021. All rights reserved.
For permissions, please e-mail: journals.
permissions@oup.com.
DOI 10.1093/ajhp/zxab070
T he electrocardiogram (ECG) is a
noninvasive study that provides
valuable information regarding both
the electrical and overall health of the
heart. Its development and imple-
mentation in clinical practice is largely
credited to Willem Einthoven’s work
on his string galvanometer electrocar-
diograph in the early 20th century.1
Because of its low cost, quick turn-
around time, and ease of perform-
ance, the ECG has become the most
frequently performed study in the car-
diology subspecialty.2 As clinical phar-
macists play an ever-increasing role in
the care of patients with confirmed or
potential cardiovascular disease, basic
ECG interpretation will become a very
helpful skill given the ECG’s utility and
widespread use. The purpose of this
primer is to introduce clinical pharma-
cists to the fundamentals of myocar-
dial cell physiology, cardiac electrical
impulse generation, electrical propa-
gation throughout the heart, and its
manifestation on the 12 lead surface
lead. ECG interpretation as it relates to
certain conditions commonly encoun-
tered by clinical pharmacists, such as
atrial fibrillation (AF), hypertension,
ischemic heart disease, ventricular
tachycardia, and QT interval prolonga-
tion, are also discussed.
Cellular physiology
The normal cellular membrane con-
sists of a lipid bilayer that is normally
impermeable to sodium, potassium,
and calcium ions. Due to concentra-
tion gradients of various electrolytes
across the cellular membrane, an elec-
trical gradient is established, with a
negatively charged environment inside
the cell and a positively charged en-
vironment outside the cell. There are
many different types of cardiac cells,
also known as myocytes, that all have
different resting electrical gradients
and properties, but the one thing they
share in common is that upon acti-
vation, they momentarily change the
charge across the membrane, eliciting

850 AM J HEALTH-SYST PHARM | VOLUME 78 | NUMBER 10 | May 15, 2021

 BASIC ECG INTERPRETATION FOR THE PHARMACIST
an action potential. Voltage-gated ion
channels sequentially open in a highly
coordinated fashion to allow ions to
traverse the normally impermeable cel-
lular membrane down concentration
and/or electrical gradients such that
there is a positively charged environ-
ment just inside the cellular membrane
and, relatively speaking, a negatively
charged environment just outside the
membrane. This sudden depolariza-
tion of cells affects adjacent excitable
tissue, depolarizing it as well. When a
wave of depolarization reaches myo-
cardial cells, the myocardial cells re-
lease calcium, which triggers muscle
contraction. After myocyte depolariza-
tion, voltage-gated ion channels also
sequentially open to repolarize the
cell and reestablish the baseline elec-
trical gradient. It is these alternating
waves of depolarizing and repolarizing
myocytes that generate the electrical
current within the chest that is re-
corded on the ECG.2
The excitable cells of the heart
can be broadly divided into myocar-
dial cells and cells of the conduction
system. Myocardial cells provide the
mechanical work required to pump
blood and cannot easily generate a car-
diac impulse on their own, while cells
of the conduction system provide no
mechanical function but are capable
of generating cardiac impulses (a pace-
maker function) and conducting car-
diac impulses. The ability to generate
cardiac impulses is due to a unique
combination of ion channels inherent
in some of types of cells of the conduc-
tion system, which is discussed below.
In contrast, other cells of the conduc-
tion system and myocardial cells lack
this unique combination of ion chan-
nels and therefore have almost no
pacemaker function.2,3
The standard ECG
The standard ECG records 10 sec-
onds of electrical activity within the
chest, and as the heart represents the
most significant source of electrical ac-
tivity in the chest, the ECG essentially
captures a 10-second electrical snap-
shot of the heart. On the vertical axis,
KEY POINTS
• The electrocardiogram is
one of the most commonly
performed tests in all of car-
diology and is unmatched
in terms of the breadth of
information provided relative
to its low cost, low risk, and
simplicity.
• Pharmacists are playing an
ever-increasing role in car-
diovascular care, and the
interpretation of electrocardio-
grams is an important skill to
possess.
• Interpreting electrocardiograms
takes practice and should be
approached consistently in a
systematic fashion.
the amplitude (in millivolts [mV]) of
the electrical activity is recorded, while
the horizontal axis represents the dur-
ation of the recording (10 seconds).
A standard, normal ECG is shown in
Figure 1.2
Sweep speed and ampli-
tude. The default speed for recording a
standard ECG is 25 mm/s (as indicated
in the bottom-left corner of Figure 1),
which is approximately 1 inch per
second and is referred to as the sweep
speed. With this setting, each “big box”
(inset) represents 200 milliseconds
(ms), while each “little box” represents
40 ms. The default scale used to re-
cord the voltage is 10 mm/mV (as indi-
cated in bottom-left corner of Figure 1);
therefore, 1 big box (5 mm) is equiva-
lent to 0.5 mV (inset).2
Limb leads, precordial leads,
and rhythm strip. While many for-
mats have been used to display a
12-lead ECG on a single page over the
years, most current machines display
data in a layout consistent with Figure 1.
The first 3 lines comprise 12 separate
individual leads (arrows), with 4 leads
per line, each occupying a quarter, or
AM J HEALTH-SYST PHARM | VOLUME 78
Primer
2.5 seconds (bracket), of the 10-second
recording. These 12 leads were de-
veloped to characterize the direction
of electrical propagation through the
heart, as well as detect regional differ-
ences among the segments of the heart,
which are discussed later.
The 6 leads in the first half of the top
3 lines (I, II, III, aVR, aVL, and aVF, in-
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dicated by narrow arrows in Figure 1)
represent limb leads, while the 6 leads
in the second half of the top 3 lines (V1
through V6, indicated by thick arrows)
represent precordial leads. The limb
leads are derived from electrodes
placed on the arms and legs, hence
the term limb leads, while the precor-
dial leads are derived from electrodes
placed around the left inframammary
line. Of the 2 leg leads, only the elec-
trode on the left leg contributes to the
limb leads; the electrode on the right
leg is the grounding lead and does not
contribute to the direction of the limb
leads because it can be placed any-
where on the body.4
The bottom 3 leads (lead V1, lead II,
and lead V5) of the ECG are referred to
as the rhythm strip leads. They present
the electrical activity recorded in a lead
throughout the entire 10 seconds of
the ECG and are most useful when at-
tempting to deduce the rhythm of the
ECG, hence their name. However, these
rhythm strip leads alone are not ad-
equate to provide information on axis,
hypertrophy, or repolarization abnor-
malities. The choice of leads to serve as
rhythm strip leads can vary but usually
includes lead II alone, leads V1 and II,
or leads V1, II, and V5.
Electrical manifestations on
the ECG
As alluded to earlier, there are 12
different leads on a standard ECG.5 In
addition to evaluation of ischemia in
specific regions of the heart, these leads
were developed to elucidate the direc-
tion of the cardiac electrical impulse
as it propagates through the heart.
Depicted in Figure 2A is a schematic of
Einthoven’s triangle, which succinctly
summarizes the location of each limb
lead. Lead I forms the top of the triangle
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 Primer BASIC ECG INTERPRETATION FOR THE PHARMACIST

Figure 1. A normal electrocardiogram (ECG). Thin arrows indicate limb leads. Thick arrows indicate precordial leads.
Brackets span 2.5 seconds, the duration of each specific lead on the ECG. The bottom 3 leads are rhythm leads and span
the entire 10 seconds of the ECG. Horizontally, each “big box” (inset) represents 200 ms, while each “small box” repre-
sents 40 ms. Vertically, each box represents 0.5 mV.

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and depicts the direction, or vector, of
the cardiac electrical impulse as it re-
lates to traveling across the chest from
a right to left direction. Any electrical
impulse that travels along this direction
(right to left) in the heart will manifest
as a positive deflection on lead I. Any
electrical impulse that travels in the
opposite direction will manifest as a
negative deflection on lead I. The amp-
litude of the deflection is a function of
both the alignment of the electrical im-
pulse with the axis of the lead (Figure 3)
as well as the mass of myocardium
being activated or deactivated. This
principle applies to all 12 leads on the
ECG, with the only variables being the
position and angle of each lead, which
are uniquely different.2
Limb and precordial lead axes.
Leads II and III form the other sides of
Einthoven’s triangle, and both are dir-
ected inferiorly towards the lower ex-
tremities. The next 3 limb leads (aVL,
aVR, and aVF) are called augmented
limb leads because one of the electrodes
for each of these leads is a “virtual elec-
trode,” with its starting position roughly
in the middle of the triangle, and the
augmented leads are then directed to-
ward the right arm (aVR), the left arm
(aVL), or the feet (aVF). The physics
behind how the location of this virtual
electrode is determined is beyond the
scope of this article. Leads aVR, aVL,
and aVF are customarily arranged adja-
cent to leads I, II, and III, respectively,
on a standard ECG.
The 6 precordial leads are named
V1 through V6, and their electrodes are
placed on the left side of the chest,
around the outside of the heart (pre-
cordium) starting just to the right of
midline (V1) and extending all the way
to the left midaxillary line (V6). (Figure
2B) For these precordial leads, another
virtual, zero-potential electrode known
as the Wilson Central Terminal, which
incorporates the voltages derived from
the limb leads, serves as the origin
of the leads, and is positioned in the
middle of the torso within the heart,
directing the axis of the precordial leads
to radiate outward from the heart to-
ward the precordium.2
Normal cardiac impulse
propagation and
manifestation on ECG
The atria of the heart serve as
“priming pumps” for the ventricles,
normally contracting approximately
120–200 milliseconds (ms) before the
ventricles to ensure the ventricles are
well filled before ejecting blood into
the pulmonary circulation, via the
right ventricle, and the systemic circu-
lation, via the left ventricle. Given this
sequence of events, it should come as
no surprise that every cardiac electrical
impulse, under normal conditions, ori-
ginates in the atria, causing the atria to
contract first, before moving onto the
ventricles. More specifically, the im-
pulse originates in the right-superior
aspect of the right atrium from a struc-
ture called the sinus node. The sinus
node is a structure that gets input from

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 BASIC ECG INTERPRETATION FOR THE PHARMACIST Primer

Figure 2. Lead placement for a standard 12-lead electrocardiogram. Panel A demonstrates limb lead locations, with the
black dot being the location of the virtual lead. Panel B demonstrates precordial lead locations using a horizontal segment
taken from the human torso (blue band), with the virtual lead circumscribed by dotted lines. The location of this virtual lead
within the body causes the vector of the precordial leads to radiate outward.

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the autonomic nervous system to deter-
mine how fast the heart rate should be;
it essentially serves as a “natural pace-
maker” for the heart. The cells in the
sinus node also depolarize more fre-
quently than any other myocyte under
normal circumstances, thus overriding
attempts by other cells in the heart to
dictate the heart rate. When each car-
diac electrical impulse originates from
the sinus node, causes atrial contrac-
tion, and then propagates to the vent-
ricles to activate the ventricles in this
chronological order, then this is con-
sidered normal sinus rhythm (NSR).
Figure 1 depicts a standard ECG during
NSR from a normal patient.2
In lead I of Figure 1, a recurring pat-
tern of a small positive deflection fol-
lowed by a larger positive deflection
is noted, representing the sequence
of events described above. The small
positive deflection represents atrial de-
polarization and is termed the P wave.
The larger positive deflection, which
occurs roughly 120 to 200 ms later,
corresponds to ventricular depolariza-
tion and is termed the QRS complex.
As alluded to earlier, the amplitude of
the deflection is dependent on both
the mass of the myocardium being de-
polarized and the direction of the elec-
trical impulse relative to the axis of the
lead in question. The P wave is much
smaller than the QRS complex because
the atria are several times less mas-
sive than the ventricles. Additionally,
as the cardiac impulse is initiated in
the sinus node and then propagates
leftward toward the left atria and vent-
ricles, the lead I P wave is positively de-
flected as well. The normal activation
of the ventricle is more complex (dis-
cussed below) but generally proceeds
in a right to left fashion and therefore
results in a positive deflection in lead
I as well. Another positive deflection is
seen after the QRS complex, and this
represents the repolarization phase of
the ventricles, termed the T wave. Each
collective P-QRS-T wave sequence rep-
resents one complete cardiac cycle, or
one heartbeat. Recognition of this pat-
tern is central to the interpretation of
the ECG.
Interpretation of the ECG
Each ECG is best approached in a
consistent, stepwise fashion to avoid
overlooking important information.
A variation on a popular systematic ap-
proach is to analyze the components of
the ECG in the following order6:
1. Rate
2. Rhythm
3. Axis and QRS characteristics
4. Intervals
5. ST changes and repolarization
abnormalities
6. Chamber hypertrophy
Rate. The heart rate, in beats per
minute (bpm) can be determined on
the standard ECG in many ways. The

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 Primer BASIC ECG INTERPRETATION FOR THE PHARMACIST

Figure 3. Panel A describes the appearance of the electrocardiogram (ECG) as it relates to the amplitude and direction of
the impulse. The direction and amplitude of the ECG is a related to the alignment of the lead to the direction of the impulse.
When the lead is parallel with the direction of the impulse, a large positive deflection is seen. Conversely, when the lead is dir-
ectly opposite to the direction of the impulse, a large negative deflection is seen. In between, varying degrees of positive and
negative deflection are seen. Panel B depicts various QRS axis deviations. Right-angle dashed lines demarcate the normal
range of QRS axes, when both lead I and aVF are upright positive on an ECG. The green arrow depicts a normal QRS axis and
corresponds to the top ECG with a green border. The purple arrow depicts a right axis deviated QRS axis and corresponds to
the middle ECG with a purple border. Note that lead aVF is upright while lead I is not. The red arrow depicts a left axis deviated
QRS axis and corresponds to the bottom ECG with a red border. Note that lead I is upright while lead aVF is not.

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A

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 BASIC ECG INTERPRETATION FOR THE PHARMACIST
easiest way is to count the number
of QRS complexes in the entire ECG,
which represents 10 seconds, and just
multiply that number by 6. This ap-
proach is especially useful when the
heart rhythm is irregular. When the
heart rhythm is regular, a faster way is
to simply divide 300 by the number of
big boxes (200 ms) between each QRS
complex. Oftentimes, the number of
boxes between QRS complexes is not a
whole number; thus it is useful to mem-
orize a few hallmark heart rates that
correspond to the distance between
QRS complexes in terms of large boxes
in whole numbers. These heart rates in-
clude 150 bpm for 2 boxes, 100 bpm for
3 boxes, 75 bpm for 4 boxes, 60 bpm for
5 boxes, and 50 bpm for 6 boxes. For in-
stance, when there are 3 to 4 large boxes
between 2 QRS complexes, the heart
rate can quickly be estimated to fall be-
tween 75 and 100 bpm, as in Figure 1.
Normal heart rate is between 60 and
100 bpm. When the heart rate exceeds
100 bpm, then tachycardia is present,
and when it falls below 60 bpm, brady-
cardia is present.
Rhythm. The rhythm of an ECG
characterizes the etiology and origin of
each heartbeat. When the distance be-
tween each QRS complex is consistent,
the rhythm can be characterized as
regular. NSR tends to be regular. When
the distance between each QRS com-
plex is erratic, the ECG rhythm should
be characterized as irregular. NSR can
also be irregular if ectopic beats from
other places in the heart interrupt the
sinus node, which will be discussed
below when discussing AF, a common
arrhythmia that exhibits a profoundly
irregular rhythm.
In addition to determining the re-
gularity of the heartbeat, it is also im-
portant to identify the origin of each
heartbeat to confirm the rhythm.
Identification of a P wave prior to
each QRS complex is paramount to
determining the origin of each heart-
beat. The 2 leads where the P wave is
most easily identifiable are leads II and
V1. During sinus rhythm, every ven-
tricular activation (ie, QRS complex) is
preceded by atrial activation (a P wave).
Equally important is to ensure the P
waves are upright (ie, propagating from
right to left) in lead I as well as upright
(ie, propagating from superior to in-
ferior) in lead aVF to confirm that atrial
activation originated from the sinus
node, which is in the top right-hand
corner of the right atrium. Thus, when
these criteria (chronological sequence
of P and QRS complexes and morph-
ology of P waves in lead I and aVF) are
met, and the rhythm is largely regular,
then the rhythm is considered NSR.
When the P wave morphology is not
upright in lead I and/or not upright in
lead aVF, then it is likely that atrial acti-
vation is originating in another area of
the atria, away from the sinus node, and
the rhythm should not be considered
NSR even if it is regular.
Axis-QRS complex. As discussed
previously, the normal cardiac im-
pulse originates from the sinus node
and then propagates to the atrioven-
tricular (AV) node, near the center of
the heart. From there, it is rapidly con-
ducted throughout the ventricles via
the His-bundle system, resulting in
near simultaneous activation of the en-
tire ventricle from the interventricular
septum out to the apex and the per-
iphery. Given the position of the heart
in the chest, the normal cardiac im-
pulse proceeds in a diagonal direction
with 2 different vectors: superior-to-
inferior and right-to-left.
The relative deflections and ampli-
tudes of the QRS complexes across the
12 standard ECG leads allow for de-
tailed characterization of the cardiac
impulse. Normally lead aVF (superior-
to-inferior) and lead I (right-to-left)
are predominantly positive, given that
the cardiac impulse proceeds from a
superior-to-inferior and right-to-left
direction (Figure 3B, green arrow). The
other leads can also serve to confirm
the direction of the cardiac impulse. For
example, lead II is better aligned with
the cardiac impulse and tends to be
more positive than either lead I or lead
aVF. Additionally, lead aVR is pointed
in the exactly opposite direction (left-
to-right and inferior-to-superior) of the
normal cardiac propagation pattern,
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hence a large negative deflection is
seen in this lead. Generally speaking,
when the QRS is upright in both lead
I and aVF, then the axis is considered
normal. Figure 3B depicts the appear-
ance of the limb leads during right axis
deviation (purple-bordered ECG), and
left axis deviation (red-bordered ECG).
Sometimes, the axis may still be con-
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sidered normal even when one of these
leads is negative, because of the rota-
tion within the heart, but borderline
axis deviation is not clinically relevant
from a pharmacist’s standpoint.
Intervals. There are 4 important
clinical intervals to inspect on an ECG:
(1) the PR interval, (2) the ORS interval,
(3) the QT interval, and (4) the ST
interval.
The PR interval (measured from the
beginning of the P wave to the onset of
the QRS) characterizes the time it takes
for an impulse to begin in the atria, tra-
verse across the AV node, and then ac-
tivate the ventricles (Figure 4A). This
value normally ranges from 120 ms to
200 ms, and corresponds with the delay
between atrial and ventricular con-
tractions. When this interval exceeds
200 ms, then first degree AV block
or delay is present. In his scenario,
there is a constant and prolonged PR
interval exceeding 200 ms (Figure 4B).
However, conduction across the AV
node can be further impaired, in both
physiologic and pathophysiologic set-
tings, to the point that atrial impulses
do not conduct down to the ventricles
in a 1:1 relationship. When this occurs,
second degree AV block is present.
Second degree AV block is commonly
divided into 2 types: Mobitz type I and
Mobitz type II. Mobitz type I is a more
benign form of AV block wherein the
PR interval steadily prolongs with
each conducted beat, resulting in the
longest PR interval just prior to the
dropped beat and the shortest PR
immediately after the dropped beat
(Figure 4C). In Mobitz type II AV block,
the PR interval is fixed during con-
ducted beats and does not vary imme-
diately before or after dropped beats.
If there is no conduction of any atrial
impulse to the ventricle, then third
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 Primer BASIC ECG INTERPRETATION FOR THE PHARMACIST

Figure 4. Intervals and segments of electrocardiograms (ECGs). Panel A depicts intervals and segments of a normal ECG.
Panel B depicts an ECG with first degree atrioventricular (AV) block with a PR interval of >200 ms. Panel C depicts an ECG
with second degree, Mobitz type I (or Wenckebach) AV block. P waves are indicated by black arrows. Note that not every
P wave (denoted by an asterisk) conducts down to the ventricles (ie, there is non-1:1 conduction). Panel D demonstrates
an ECG with complete AV block. The ventricles, beating at 40 bpm, are completely dissociated from the P waves (black
arrows), which indicate the atria are beating at close to 140 bpm. Complete AV dissociation is present here.

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degree, or complete, AV block is pre-
sent (Figure 4D). In this setting, the PR
interval will be irregular, and there will
be no pattern of association between P
waves and QRS complexes (this is re-
ferred to as complete AV dissociation).
Mobitz type II and third degree AV
block are considered high-grade AV
blocks and will usually require per-
manent pacemaker implantation.7 For
a more detailed discussion of AV block,
please refer to Braunwald’s Heart
Disease: A Textbook of Cardiovascular
Medicine.2
The QRS interval characterizes the
time to activate the ventricles. During
normal conduction, ventricular acti-
vation proceeds rapidly through the
His-Purkinje system (HPS), a net-
work of highly specialized conduction
cells interspersed among the ven-
tricular myocardium. The rapid con-
duction of a cardiac impulse down
the HPS enables the heart to contract
synchronously, thereby optimizing
the ejection of blood out of the vent-
ricles. When this occurs it is mani-
fested on an ECG with a narrow QRS
complex (<120 ms). When the car-
diac impulse fails to conduct down
the HPS, ventricular activation is
dyssynchronous and manifests on the
ECG with a QRS complex that is wider
than 120 ms. This can occur when ei-
ther the right or left bundle branch
of the His bundle pacing system is
damaged or malfunctioning, causing
right bundle branch block (RBBB)
and left bundle branch block (LBBB),
respectively.
The QT interval represents the total
time it takes to depolarize and fully
repolarize the ventricles. It is measured
from the beginning of the QRS complex
to the end of the T wave, as measured
on the lead with the latest T wave.8 An
excessively short or long QT can result
in serious arrhythmias, and several
classes of drugs can significantly alter
the QT interval.
Because the heart rate can dramat-
ically change the QT interval, the QT
interval is commonly “corrected” via
several commonly used formulas to
standardize the interval in the setting
of different heart rates.9 The heart rate–
corrected QT interval (QTc) is generally
considered short if it is less than 390 ms
and is considered long if it exceeds
460 ms in women or 450 ms in men.10
The ST interval is important be-
cause it provides valuable information
on the repolarization status of the heart.
Changes such as elevation or depression
are more important than the actual dur-
ation of this segment. Repolarization ab-
normalities and chamber hypertrophy
are discussed below.
Although the suggested order of
components to be analyzed is not abso-
lute, it is important to practice consist-
ency by using one stepwise approach

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 BASIC ECG INTERPRETATION FOR THE PHARMACIST
every time to ensure every ECG is
methodically interpreted.
Clinical applications
Atrial fibrillation. AF is the most
common sustained arrhythmia and
occurs when the atria fibrillate several
hundred times a minute instead of syn-
chronously contracting 60 to 100 times
a minute.11 The diagnosis of AF centers
around the use of the ECG as a means of
both screening and confirmation. The
hallmark of AF on the ECG is an “irregu-
larly irregular” rhythm with an absence
of organized P waves. A clear, recog-
nizable pattern of recurring P waves
or QRS complexes is almost uniformly
absent due to the erratic nature of the
fibrillation, and the QRS complexes are
often described as irregularly irregular.
Figure 5A depicts an ECG of a patient
in sinus rhythm with premature atrial
complexes (PACs). PACs occur when a
piece of atrial tissue initiates an elec-
trical impulse before the sinus node ini-
tiates a cardiac impulse. The rhythm of
this ECG is irregularly regular because
the rhythm is predominantly regular
throughout, with intermittent periods
of irregularity that are unpredictable.
Figure 5B depicts an ECG of a patient
in sinus rhythm with premature ven-
tricular complexes (PVCs). PVCs occur
when a piece of ventricular tissue ini-
tiates an electrical impulse before the
cardiac impulse from the sinus node
reaches the ventricles. The rhythm of
this ECG is “regularly irregular.” Periods
of irregularity are present throughout
the ECG, but they occur at set intervals
that are rather predictable (in this case,
every fourth beat). When PVCs occur
every fourth beat, the rhythm is char-
acterized as ventricular quadrigeminy.
When PVCs occur every third beat or
second beat, then they are referred to
as ventricular trigeminy or bigeminy,
respectively. Finally, Figure 5C depicts
an ECG of a patient with AF. Irregularity
is largely present throughout the entire
ECG, with some portions being more ir-
regular than others, and it is impossible
to predict the degree of irregularity at
any given time. Additionally, the fibril-
lation also lowers the amplitude of the
P waves, and sometimes they can be
completely absent. Although this ECG
clearly demonstrates AF, the ECGs of
some patients with AF are not always
easy to decipher. Since accurate inter-
pretation of the ECG is central to the
management of AF, it may be prudent
to ask for a second opinion when the
rhythm of the ECG is unclear.
Ischemic heart disease. Identi­
fication of ischemia is perhaps one
of the most powerful applications of
the ECG. Cardiac ischemia is detected
by inspecting the ST segment and T
wave, which correspond to ventricular
repolarization, for repolarization ab-
normalities. The ST segment and the
TP segment are usually on the same
level, or isoelectric relative to one an-
other (as in Figure 4A). The 12 standard
ECG leads can be grouped together
based on the regions or “territories”
of the heart they represent from the
standpoint of repolarization abnormal-
ities. Leads II, III, and aVF correspond
to the inferior portion of the heart,
and perfusion there is predominantly
supplied by the right coronary artery.
Leads V1 through V4 correspond to the
anterior portion of the heart, including
the septum, and perfusion there is sup-
plied by the left anterior descending
artery. Finally, leads I, aVL, V5, and V6
correspond to the lateral portion of
the heart, where perfusion is predom-
inantly supplied by the left circumflex
artery. Repolarization abnormalities
in these leads suggest that cardiac is-
chemia may be present in the corres-
ponding territories of the heart.
Repolarization abnormalities can
pragmatically be divided into injury
patterns (ST-segment elevation) or is-
chemia pattern (ST-segment depres-
sion or T-wave inversions). When acute
ischemia in a territory becomes so se-
vere that myocardial injury occurs, the
ST segment becomes elevated rela-
tive to the TP segment in those leads
(Figure 5). The degree of ST elevation
that is considered significant depends
on age, gender, and the lead(s) affected
(Table 1) but is generally considered
to be 0.1 mV. ST-segment elevations
are usually seen in more than one
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contiguous lead within a territory when
indicative of myocardial injury, such as
that caused by ST-elevation myocar-
dial infarction (STEMI) in acute cor-
onary syndrome (ACS). It is unusual
to have simultaneous ST elevations
in more than one territory due to car-
diac ischemia. ST elevation resulting
from other causes, especially when
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present in all 3 territories, is generally
not due to ischemia and is more likely
a result of pericarditis or benign early
repolarization. Pericarditis is a condi-
tion in which the pericardium, a mem-
brane surrounding the heart, becomes
inflamed. This inflammation can cause
profound repolarization abnormal-
ities (ST elevations and depressions,
as well as T-wave changes) on the ECG,
usually involving all territories of the
heart. Thus, it is important to differen-
tiate pericarditis from STEMI because
ST elevation due to myocardial injury
caused by ACS is a medical emergency
that often requires endovascular inter-
vention in a cardiac catheterization la-
boratory, while pericarditis is generally
managed medically.2
Cardiac ischemia, including un-
stable angina or demand ischemia,
that has not resulted in myocardial in-
jury tends to manifest with ST-segment
depression and T-wave changes,
not ST-segment elevations.12 These
changes, as with ST elevations, tend
to occur in certain territories of the
heart that are supplied individually by
major coronary arteries, so a pattern
of changes among contiguous leads
within a region is usually observed
if ischemia is present. Other clinical
scenarios, such as electrolyte abnor-
malities, and certain medications can
also cause ST-segment depressions and
T-wave changes, but these tend to af-
fect leads that extend beyond just one
territory of the heart, and the changes
are often not in contiguous leads.8
T-wave changes such as inverted, or
“flattened,” T waves can also represent
cardiac ischemia, but such changes are
generally considered less specific than
ST-segment depression, especially in
the case of minor T-wave changes.8
In adults, T waves are inverted in lead
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 Primer BASIC ECG INTERPRETATION FOR THE PHARMACIST

Figure 5. Irregular rhythms. Panel A demonstrates an electrocardiogram (ECG) with frequent premature atrial complexes
that result in rhythm that is irregularly regular. Panel B demonstrates an ECG with frequent premature ventricular com-
plexes that result in a pattern of ventricular quadrigeminy that is regularly irregular. Panel C demonstrates an ECG with
atrial fibrillation. The hallmark of atrial fibrillation is an irregularly irregular rhythm with an absence of organized P waves.

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B

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 BASIC ECG INTERPRETATION FOR THE PHARMACIST
Figure 5. Continued
Table 1. Threshold Values for Ischemic ST-Segment and T-Wave Changes
Type Definition
ST elevation12
Men Elevation in 2 contiguous leads by >0.1 mV in all leads ex-
cept V2 and V3; for leads V2 and V3, elevation of >0.2 mV
in men older than 40 years of age or >0.25 mV in men
younger than 40
Women Elevation in 2 contiguous leads by >0.1 mV in all leads ex-
cept V2 and V3; for leads V2 and V3, elevation of >0.15 mV
ST depression19 Horizontal or down-sloping depression of >0.05 mV in 2
contiguous leads
T-wave changes19 Inversion of >0.1 mV in 2 contiguous leads along with prom-
inent R wave
aVR and can be inverted in leads III, Ventricular tachycardia. Ventric­­
aVL, and V1; T waves are upright in the ular tachycardia (VT) is a dangerous
other leads. The degrees of ST-segment arrhythmia involving cardiac impulses
depression and T-wave changes that that originate from within the vent-
are considered abnormal are listed in ricles instead of the sinus node. The
Table 1. Although the ECG can aid in electrocardiographic hallmark of this
the diagnosis of myocardial ischemia, arrhythmia is tachycardia with a wide
it should always be supplemented with QRS complex, referred to as wide com-
a thoughtful history and a review of la- plex tachycardia (WCT).2 The QRS is
boratory values and should never be wide in VT because the arrhythmia
used in isolation to make a diagnosis of will generally bypass the HPS, in-
ischemia. stead relying on myocyte-to-myocyte
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conduction throughout the ventricles.3
This arrhythmia is often rapidly fatal
unless it is quickly terminated because
the rapidity and desynchrony of this
arrhythmia afford very little cardiac
output. It is important to note that not
all WCT is VT, as many supraventricular
etiologies can also cause WCT, such as
in the setting of baseline RBBB, base-
line LBBB, or aberrancy, which is
when the HPS is overwhelmed and
conduction is no longer over the en-
tire HPS. Differentiating VT from
supraventricular etiologies is beyond
the scope of this article, and many ECG
algorithms have been developed to dis-
tinguish these sources of WCT.13
Left ventricular hypertrophy
and hypertension. As alluded to
earlier, the amplitude of the deflections
on the ECG is affected by the mass of
the myocardium being depolarized
or repolarized. Patients with left ven-
tricular hypertrophy (LVH) usually
meet ECG voltage criteria for LVH, and
this can provide information on both
the chronicity and control of elevated
blood pressure in patients with es-
sential hypertension. As patients with
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 Primer BASIC ECG INTERPRETATION FOR THE PHARMACIST

Figure 6. Spurious automated measurement of the heart rate–corrected QT interval (QTc). This electrocardiogram (ECG)
was incorrectly interpreted by the acquisition system as having a prolonged QT interval. The T wave amplitudes in this
ECG were high and being counted as another QRS complex, effectively doubling the actual heart rate of the ECG from 74
bpm to 148 bpm (see ellipse). As a result, the QTc was calculated to be 524 ms (black box) when it was actually 431 ms
after adjusting for a heart rate of 74 bpm.

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hypertension are usually asymptomatic,
providing them with tangible evidence
that their body is being adversely af-
fected by high blood pressure may help
with compliance. There are well over
30 different published voltage criteria
for LVH, but 2 common criteria used
in clinical practice are the Cornell and
the Lyon-Sokolow criteria.14,15 For the
Cornell criterion, LVH is present when
the sum of the amplitude of the S wave in
V3 and the R wave in aVL exceeds 20 mm
in women and 28 mm in men. For the
Lyon-Sokolow criterion, LVH is present
when the sum of the S wave in V1 and the
R wave in V5 or V6 exceeds 35 mm.
Long QT interval. Prolongation
of the QT interval can be congenital
or acquired, but regardless of the eti-
ology, dangerous ventricular arrhyth-
mias can arise from a prolonged QT
interval. Generally speaking, the longer
the QT interval, the greater the risk of
sudden cardiac death, and there is no
minimum QT interval at which there
is no risk of ventricular arrhythmias.16
Because pharmacists often serve as the
“last line of defense” in verifying medi-
cations just prior to dispensing, they
play a crucial role in preventing iatro-
genic ventricular arrhythmias due to
QT interval prolongation, as patients
often have multiple practitioners and
consultants taking care of them.
The QTc is uniformly calculated by
most modern ECG acquisition systems.17
These automatic measurements are
usually very accurate, but peaked T
waves (Figure 6), U waves, or artifacts
can sometimes yield spurious results.18
It is not unreasonable to manually check
the QTc by measuring the QT interval
and verifying the heart rate has been ac-
curately recorded by the system, as these
are the variables used by the automated
system to calculate the QTc.
Conclusion
The ECG has been one of the most
useful, and yet simplest, diagnostic
tools in the subspecialty of cardiology
since Willem Einthoven’s development
of the string galvanometer electrocar-
diograph in the early 20th century.1 Few

860 AM J HEALTH-SYST PHARM | VOLUME 78 | NUMBER 10 | May 15, 2021

 BASIC ECG INTERPRETATION FOR THE PHARMACIST
studies in cardiology can offer the clin-
ician the breadth of information pro-
vided by the ECG, with other benefits
including its low cost to the healthcare
system, low risk to the patient, and fast
turnaround time in terms of study per-
formance and interpretation.
Disclosures
The authors have declared no potential con-
flicts of interest.
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