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1
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Y. Alz a i d i
Chapter 2
Approach toECG Interpretation
inCritical Care
MiguelH.Vicco, DaniloWeirRestrepo, ShylaGupta, JuanM.Farina,
LeandroLuisPozzer, FernandaTavares-Da-Silva, SebastiánGarcia-Zamora,
AlejandroNarváezOrozco, AndresF.Miranda-Arboleda,
andAdriánBaranchuk
2.1 Introduction
Since 2015, Advanced Cardiac Life Support guidelines have emphasized the importance of pharmacists being involved in cardiac emergencies to minimize the risk of
medication-related errors, drug adverse reactions, and mortality [1, 2]. Based on
M. H. Vicco
Drug Safety Lead, Organon BV, Brussels, Belgium
D. W. Restrepo
Internal Medicine Resident, CES University, Medellín, Colombia
S. Gupta
Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada
J. M. Farina
Division of Cardiothoracic Surgery, Mayo Clinic, Phoenix, AZ, USA
L. L. Pozzer
Section of Cardiac Electrophysiology, Buenos Aires Cardiovascular Institute,
Buenos Aires, Argentina
F. Tavares-Da-Silva
Drug Safety, Organon BV, Brussels, Belgium
S. Garcia-Zamora
Coronary Care Unit, Delta Clinic, Rosario, Argentina
A. N. Orozco
University of Antioquia, Medellín, Colombia
A. F. Miranda-Arboleda
Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA
A. Baranchuk (
Division of Cardiology, Queen’s University, Kingston, ON, Canada
e-mail: Adrian.Baranchuk@kingstonhsc.ca
*)
Switzerland AG 2025
Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical
Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_2
29© The Author(s), under exclusive license to Springer Nature
30
M. H. Vicco et al.
this, the Heart Rhythm Society’s 2015 Statement on Clinical Cardiac
Electrophysiology suggests that pharmacists should be trained in electrocardiogram
(ECG) interpretation [2].
It is worth noting that not all pharmacists will practice in acute care settings.
However, considering the growing involvement of pharmacists in the care of patients
diagnosed with cardiovascular disease or at risk of developing it, understanding
electrocardiograms (ECGs) is important. Moreover, given the relevance of druginduced ECG alterations, pharmacists must be capable of independent ECG interpretation. The goal of this chapter is to provide a reference tool for pharmacists on
ECG normal parameters and main ECG abnormalities concerning for the pharmacists involved in patient care in different settings.
2.2 Normal Conduction System andPhysiology
To accurately interpret an ECG, it is imperative to have a comprehensive understanding of the heart’s electrical system [3, 4].
Two key characteristics of the heart include its intrinsic capability to produce
electrical impulses independently, a phenomenon known as automaticity, and its
unique electrical structure, consisting of the sinoatrial (SA) node, the atrioventricular (AV) node, and the His-Purkinje system [3, 4]. Cardiac cells demonstrate a
degree of specialization, with some cells being better at generating electrical signals
(such as those in the SA and AV nodes), some being more conductive (like those in
the His- Purkinje system), and some being primarily responsible for contraction (the
muscular cells).
Typically, the cardiac cycle begins at the SA node, which acts as the pacemaker
[3, 4]. From there, the electrical signal travels to the AV node, which serves as the
only pathway for the impulses to reach the ventricles under normal circumstances.
The AV node acts as a lter, preventing abnormal impulses from reaching the ventricles. Following the AV node, the His-Purkinje system takes over, specializing in
the conduction of impulses. This system is divided into the right bundle branch and
the left bundle branch. The left bundle branch splits into the anterior, septal, and
posterior fascicles. Finally, the His-Purkinje system further divides into numerous
microbers, ensuring that the electrical impulse reaches the entire inner surface of
the ventricles almost simultaneously.
The generation and propagation of electrical signals in cardiac cells are facilitated by their ability to control the opening and closing of numerous ion channels
present in their membranes [3, 4]. The typical structure of a cellular membrane is
composed of a lipid bilayer, which typically does not allow the passage of sodium,
potassium, and calcium ions. As a result of the concentration differences of different
electrolytes across the cellular membrane, an electrical gradient is formed. This creates a negatively charged interior environment within the cell and a positively
charged exterior environment surrounding the cell. Depending on the specic type
of cardiac cell, the ion channels possess a complex structure. These ion channels
2
Approach toECG Interpretation inCritical Care
31
will exhibit distinct resting electrical gradients and properties (Table2.1). However,
despite these differences, they all share a common characteristic. When activated,
they undergo a temporary alteration in the charge across their membrane, resulting
in the generation of an action potential.
This normal action potential can be illustrated in ve phases (Fig.2.1):
• Phase 4—Resting membrane potential.
• Phase 0—Rapid depolarization.
Table 2.1 Types of ion channels and their function
Voltage-gated sodium channels (Na+):
Predominantly found in cardiac myocytes.
During the initial phase of the cardiac cycle, voltage-gated sodium channels play a pivotal
role in depolarizing cardiac myocytes.
Upon membrane depolarization, these channels rapidly open, allowing an inux of sodium
ions into the cell (phase 0), resulting in the rapid upstroke of the action potential.
This depolarization phase initiates myocardial contraction and f
electrical impulses throughout the heart.
L-type calcium channels (Ca
Expressed in cardiac myocytes and cardiac pacemaker cells.
L-type calcium channels are critical for sustaining myocardial contraction during the plateau
phase of the action potential.
Upon activation by membrane depolarization, these channels facilitate calcium inux into
cardiac myocytes (phase 2), leading to an increase in intracellular calcium concentration.
vated intracellular calcium triggers the release of additional calcium from the sarcoplasmic
Ele
reticulum, facilitating excitation-contraction coupling and promoting myocardial contraction.
Voltage-gated potassium channels (K
Abundantly present in cardiac myocytes.
V
oltage-gated potassium channels are responsible for repolarizing cardiac myocytes during
the latter phases of the cardiac cycle.
F
ollowing depolarization, these channels open, allowing potassium efux from the cell,
thereby restoring the negative resting membrane potential (phases 1, 2, and 3).
Repolarization of the cardiac myoc
for subsequent contraction.
Inward rectier potassium channels (Kir):
Predominantly e
Inw
ard rectier potassium channels play a role in stabilizing the resting membrane potential
and modulating pacemaker activity in cardiac pacemaker cells.
These channels permit potassium inux during membrane h
the maintenance of the resting membrane potential and the regulation of the pacemaker ring
rate.
By modulating the e
contribute to the initiation and regulation of the cardiac rhythm.
Ryanodine receptors (RyRs):
Ryanodine receptors are located on the sarcoplasmic reticulum in cardiac myocytes and play
a crucial role in calcium-induced calcium release.
Acti
vation of RyR channels leads to the release of calcium ions from intracellular stores in
response to increased intracellular calcium concentration.
This calcium release mechanism f
synchronized myocardial contraction and effective ejection of blood from the ventricles.
xpressed in cardiac pacemaker cells.
2+):
+
):
ytes enables myocardial relaxation and prepares the heart
xcitability of pacemaker cells, inward rectier potassium channels
acilitates excitation-contraction coupling, ensuring
acilitates the propagation of
yperpolarization, contributing to
32
Fig. 2.1 Phases of the
normal action potential and
its correlation with the
cardiac cycle in the ECG
M. H. Vicco et al.
• Phase 1—Early repolarization.
• Phase 2—Plateau.
• Phase 3—Rapid repolarization.
2.3 Formation ofthe12-Lead ECG
The ECG is a visual representation detailing the spatial orientation and electrical
activity produced during the depolarization and repolarization phases of the heart’s
atria and ventricles [3–5]. This electrical activity is captured by electrodes afxed to
the skin. For example, if the electrical vector is approaching the electrode, this
results in a positive deection on the ECG.Inversely, if the electrical activity moves
away from the electrode, this results in a negative deection on the ECG.If the
“observer” electrode is in the middle and rst sees it approaching and then moving
away, a signal will be drawn initially positive and then negative.
The conventional 12-lead ECG is obtained by placing 10 electrodes on the
patient:
• Four limb electrodes (located in the vertical or frontal plane axis) are placed on
the right arm (red), left arm (yellow), right leg (black), and left leg (green). These
electrodes will give rise to six leads, i.e., I, II, and III (bipolar leads) and aVR,
aVL, and aVF (unipolar leads).
• Six precordial electrodes (located in the horizontal plane axis) which will give
rise to the precordial leads V1, V2, V3, V4, V5, and V6 (unipolar) are placed as
follows:
– V1: fourth intercostal space, right parasternal line.
– V2: fourth intercostal space, left parasternal line.
– V3: between V2 and V4.
– V4: fth intercostal space, left midclavicular line.
– V5: fth intercostal space, left anterior axillary line.
– V6: fth intercostal space, left midaxillary line.
2
Approach toECG Interpretation inCritical Care
33
Each of the 12 leads represents a particular orientation in space, to capture spatial
information of the heart’s electrical activity in three orthogonal directions, right to
left and left to right; superior to inferior and inferior to superior; and anterior to
posterior and posterior to anterior [3–5].
The horizontal plane is constituted by the unipolar precordial leads, consisting of
a positive electrode that will show the posterior to anterior (V1, V2, and V3) or right
to left-lateral (V4, V5, and V6) spatial information of the heart’s electrical activity.
In the frontal plane, the 6 leads will constitute the hexaxial reference systems,
which measures a copulate circle or 360 degrees around the heart. The hexaxial
reference system is a geometric representation used to interpret the direction of the
electrical vectors in this plane.
2.4 ECG Nomenclature
A normal ECG (Figs.2.2 and 2.3) is comprised of the following elements [3–5]:
• Wave: A deviation (deection) either above (positive) or below (negative) the
baseline indicating a distinct electrical occurrence. The ECG depicts several
waves, namely P, Q, R, S, T, and U waves.
• Interval: The duration between two ECG waves. Commonly assessed intervals
include the PR, QRS (or QRS duration), QT, and RR.
Fig. 2.2 Normal ECG
nomenclature, waves,
segments, and intervals
34
Fig. 2.3 Normal ECG. Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG WaveMaven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
M. H. Vicco et al.
• Segment: The length between two specic ECG waves that are expected to be at
a baseline amplitude (neither positive nor negative). The main segments include
the PR and ST segments.
• Complex: A cluster of multiple waves amalgamated together. The principal complex discernible on an ECG is the QRS complex.
• Point: Singularly identied as the J point, this point marks the transition from the
QRS complex to the ST segment.
2.4.1 P Wave
The rst element observed on an ECG during a normal cardiac cycle is the P wave
[3–5]. The P wave represents atrial depolarization. Therefore, its presence indicates
that the patient is in sinus rhythm. As a typical atrial impulse begins in the sinoatrial
node, situated in the upper right region of the right atrium, the propagation of the
activation front occurs from top to bottom and from right to left. This results in a
positive P wave in lead I and II and a negative P wave in aVR.Usually, the P wave
is also positive in lead III, aVF, and aVL, although this may differ based on the
heart’s orientation within the chest cavity.
Normal P waves typically last less than 100ms and have a height of less than
2.5mm (0.25mV). Also, they may be bid, mainly in the precordial leads, because
of a slight asynchrony between the depolarization of the right and left atria. The
peak-to-peak length is <1 mm, but if longer, this delayed conduction suggests a
pathological condition, as the case of interatrial blocks.
2 Approach toECG Interpretation inCritical Care
35
2.4.2 PR Interval
The PR interval on an ECG represents the time interval from the beginning of atrial
depolarization (start of the P wave) to the beginning of ventricular depolarization
(start of the QRS complex) [3–5]. Thus, it reects the time it takes for the electrical
impulse to travel from the atria through the AV node to the Purkinje system, just
before ventricular contraction.
The PR interval should not be confused with the PR segment, as the PR segment
represents a period of electrical quiescence between atrial and ventricular depolarization. The PR segment extends from the end of the P wave to the beginning of the
QRS complex.
The normal PR interval typically ranges from 120 to 210ms; this duration can
vary slightly based on factors such as age or heart rate.
It is important to note that typically, PR interval duration corresponds to the AV
node. This is dependent on adrenergic tone, which can slow down or accelerate
conduction. Thus, in the context of AV node dysfunction, or medications that alter
the normal function of the AV node, the PR interval may also be prolonged.
2.4.3 QRS Complex
The next wave observed on the ECG is the QRS complex which provides information for understanding how electrical activity spreads through both ventricles (ventricular depolarization) [3–5].
The QRS complex represents a combination of three waves: Q for the rst nega-
tive deection, R for the rst positive deection, and S for the second negative
deection, with subsequent positive or negative deections marked as R’ or r’ and
S′ or s’. A normal QRS complex can start with a Q wave that is not wider than 40ms
or 30% of the QRS height. A normal Q wave typically appears without notches and
separates sharply from the baseline. The R wave is usually taller in limb leads compared to precordial leads. The characteristics of each wave constituting the QRS
complex can be summarized as follows:
The QRS interval is usually narrow (<100ms) due to rapid simultaneous activa-
tion of both ventricles. However, if there is a blockage in the conduction system, a
myocardial scar, or other conditions, it may widen (>120ms). Besides its length, it
is important to determine its axis as it reveals crucial information regarding the
orientation of cardiac electrical activity within the body. Deviations from the normal
axis serve as pivotal indicators of diverse cardiac pathologies, including ventricular
hypertrophy, bundle branch blocks, or myocardial infarction. Under normal circumstances, the normal axis falls between −15° and +105°. The QRS axis is calculated
by examining the net direction of electrical depolarization in the heart during ventricular activation, which is primarily represented by the QRS complex on an
ECG.There are several methods to determine the QRS axis; however, the most used
ones are the following:
36
M. H. Vicco et al.
1. Quadrant method: This approach involves plotting the net QRS vectors from
leads I and aVF on a graph with two axes, with one representing lead I and the
other representing lead aVF. The intersection of these vectors indicates the
approximate location of the QRS axis.
2. Isodirectional method: In this method, the leads showing the most isoelectric
QRS complexes (neither predominantly positive nor negative) are identied. By
determining the lead with the isoelectric QRS complex and observing its relation
to other leads, the QRS axis can be estimated.
Abnormal axis deviation, indicating the underlying pathology, can be schemati-
cally divided into the following categories:
• Left axis deviation=QRS axis less than −30°.
• Right axis deviation=QRS axis greater than +90°.
• Extreme axis deviation=QRS axis between −90° and 180°.
In summary, understanding the characteristics of the Q, R, and S waves on an
ECG is essential for accurate interpretation. While these waves often exhibit normal
variations, pathological changes may indicate underlying cardiac abnormalities
such as myocardial infarction, hypertrophy, or conduction disturbances.
2.4.4 J Point
The J point represents the junction between the termination of the QRS complex
and the beginning of the ST segment [3–5]. It holds signicant clinical relevance as
it serves as a reference point for assessing myocardial depolarization and initiation
of ventricular repolarization.
Under normal physiological conditions, the J point should be precisely aligned
with the baseline (isoelectric), indicating that ventricular depolarization has been
completed, and repolarization is commencing.
However, deviations from this normative pattern can occur, potentially indicat-
ing pathological processes, such as the following:
ST
-segment elevation: A J point that is elevated above the baseline by at least
•
1mm (mV) in two contiguous leads (or 2.5mm in V2–V3in men under 40years,
or 2mm in men over 40years or in women) is indicative of ST-segment elevation. This nding is often associated with acute myocardial infarction (AMI) and
requires urgent medical attention.
• ST-segment depression: Conversely, J point depression and an ST segment below
the baseline may be considered pathological if it exceeds 0.5mm in two contiguous leads. This nding can indicate myocardial ischemia and may be observed in
conditions such as unstable angina or non-ST-segment elevation myocardial
infarction (NSTEMI). ST-segment depression may also occur in other nonischemic conditions such as left ventricular hypertrophy or the digitalis effect.