Learning Objectives: Chapter 4: Electrophysiology of The Heart

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15/3/2020

Cardiology: An Integrated Approach

Chapter 4: Electrophysiology of the Heart

Learning Objectives
Learning Objectives

By the end of the chapter the student will be able to:

Draw a typical action potential in a ventricular muscle and a pacemaker cell.

Describe the ionic basis of the phases of the action potential.

Explain the significance of the long duration of the cardiac action potential and the resultant long refractory period.

Describe the normal sequence of cardiac activation and conduction and predict the consequence of its abnormalities.

Discuss the significance of “overdrive suppression” in a natural pacemaker and the abnormalities leading to an “ectopic pacemaker.”

Explain the e ects of the sympathetic and parasympathetic nervous system on the heart rate, cardiac conduction, and contractility.

Describe the main components of a normal ECG recording, their significance, and abnormalities.

Introduction
The contraction and relaxation of the cardiac muscle follows a specific synchronized pattern between the atria and the ventricles. This rhythmic contraction and
relaxation is preceded by electrical activity called the action potential that is represented in the depolarization and repolarization of the cardiac muscle,
respectively. The special origin and sequence of the initiation and propagation of the action potential is essential for maintaining normal heart function. The action
potential is created by ions fluxes across the plasma membrane of the cardiac muscle cells via specific channels, transporters, and other proteins. Normally, the
action potential originates in the sinoatrial (SA) node known as “the pacemaker of the heart,” which propagates a specific sequence in the atria first and then in the
ventricle through specialized conducting tissues as shown in Fig. 4.1. Although the SA node activity sets up the heart rate, the autonomic nervous system
modulates this heart rate as well as the electrical conduction and contraction of the heart. Electrical activities of the heart can be precisely measured and
monitored via electrocardiography (ECG). Any disturbances of the heart electricity result in various types of arrhythmias as discussed in Chapter 9, which can lead
to serious consequences including death. This chapter will briefly explain the major components of the electrical activity of the heart and how it is regulated and
measured.

Figure 4.1
Sectional view of the heart. The basic anatomy of the heart is indicated, including chambers, major blood vessels, and conducting system (yellow), including the
sinoatrial node, atrioventricular node, and Purkinje fibers. (Reproduced, with permission, from Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of
Medical Physiology. 24th ed. New York: McGraw-Hill; 2012.)

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Origin and Pathway of the Action Potential of the Heart


There are 3 types of cardiac muscles according to their excitability: (1) the pacemaker cells, (2) the conducting tissues (bundle of His, Purkinje fibers), and (3) the
ventricular and atrial muscle fibers. Each of these types has its unique action potential as will be discussed. In general, the action potential originates in the SA
node and then spreads to both the atrial nodes via the internodal tracts and the atrial tissues. Then, the action potential passes to the atrioventricular (AV) node
and to the ventricle through bundles of His and Purkinje fibers. The conduction of the action potential in the AV node is much slower than in any other part of the
heart. This conduction delay in the AV node is important as it allows the atria to contract before the ventricle, so that the ventricle completely fills with blood before
it contracts and ejects the stroke volume. Therefore, any shortening of the AV node conduction can result in less ventricular filling and reduce the stroke volume
and the cardiac output. The electrical insulation between the atria and the ventricle is critical for preventing electrical conduction other than through the AV node
and the bundle of His. This insulation is achieved by fibrous tissue that surrounds the tricuspid and mitral valves as shown in Fig. 4.2. Once the action potential
passes the AV node, it spreads very quickly through a common bundle of the His, then to the right and le bundle branches to the Purkinje fibers, and finally to the
ventricle tissues from the endocardium to the epicardium. The action potential normally travels in one direction. The fast travel of the action potential in the His-
Purkinje fibers allows the ventricles to function as one unit, known as functional syncytium. This rapid spreading of the action potential across the cardiac tissues is
due to a large number of gap junctions in the intercalated discs that is unique to the heart.

Figure 4.2
Fibrous tissues encircle the tricuspid and mitral valves as well as the great vessels between the atria and the ventricles and serve as electrical insulator to allow the
action potential to travel only through the AV node and the AV bundle and also as a valve support.

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Basic Principles of the Action Potential

The ion movement across the plasma membrane is the basis for the action potential, especially Na+, K+, and Ca2+. In a normal cardiac cell, the Na+ and Ca2+
concentrations are much higher in the extracellular fluid, while the K+ concentration is higher in the intracellular fluid. Ion transport across cell membranes is
governed by the concentration gradient, the transmembrane electrical potential, as well as the permeability of the plasma membrane. The ions move from a high
concentration area to a lower concentration area, so the higher the concentration gradient, the higher the rate of the ion flow. At the resting state of the cardiac
cells, the Na+ concentration is much higher outside the cell compared to inside the cell, it is about 145 mM vs.15 mM, respectively. Therefore, there is a strong
tendency of the Na+ to move inside the cell down to its concentration gradient. Furthermore, the resting transmembrane potential of the cardiac cell is
approximately -95 mV with the negative charge inside the cell relative to the outside of the cell. This negative charge inside the cardiac cell attracts the positively
charged Na+ ions. These two forces, the concentration gradient, and the electrical potential promote the strong tendency of the Na+ ions to enter the cell during
depolarization of the action potential.

The third critical factor that determines the ion transport across the plasma membrane is a change in the membrane permeability, or the ion conductance. The
phospholipid bilayer membrane is not permeable to ions; instead, special ion channels within the membrane allow the ions to pass across the membrane when it is
open. The majority of the ion channels consist of repeating transmembrane domains of glycosylated proteins. The channels are characterized by their selectivity to
a specific ion and by their gating properties, which are either opened or closed for certain periods of time. The opening and closing of the channel gate is
determined by the voltage or legend depending on the type of the channels. A good example for a voltage-sensitive gating channel is the fast sodium channel,
which causes depolarization.

The membrane potential of cardiac cells depends on the conductance of the ions and the concentration and electrical gradients of those ions across the cell
membrane. When the conductance of a specific ion is high, this ion will flow down to its electrochemical gradient and will drive the membrane potential toward its
equilibrium gradient according to the Nernst equation. The ions with low conduction will have almost no e ect on the membrane potential. In a cardiac cell, the
resting membrane potential is mainly determined by K+ ions because its conductance is very high (via the inward rectifier of the potassium channels) which result
in K+ outward movement. As a consequence, the resting membrane potential is close to the equilibrium potential of the K+ ions which is –91 mV according to the
following Nernst equation, considering that at rest, K+ concentration in the intracellular fluid is about 150 mM and in the extracellular fluid is 5 mM:

Potassium equilibrium potential = –26.7 In ([K+]in / [K+]out) = –91 mV


 

The Na+-K+ ATPase pump mainly maintains the Na+ and K+ ion concentration potential across the cell membranes, but also plays a minor role in contributing to the
membrane potential.
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The Action Potential of the Cardiac Muscle Cells (Ventricles, Atria, and Purkinje Fibers)

The action potential in all cardiac muscle cells except that the SA and AV nodes share similar characteristics, such as longer duration, plateau, and stable resting
membrane potential, as shown in Fig. 4.3. The longest duration is in the Purkinje cells, at about 300 ms, followed by 250 msec in the ventricles, and 150 msec in the
atria. In general, those durations are much longer compared to the very short duration of the action potential in the skeletal muscle and the nerve cells, which are
about 1 to 2 msec. In contrast to the SA and AV node cells, the resting membrane potential of cardiac cells, if not stimulated, remains stable at –90 mV as indicated
in phase 4 below. The ionic basis of each phase of the action potential is described in detail below and illustrated in Fig. 4.4A.

Figure 4.3
Conducting system of the heart. Typical transmembrane action potentials for the SA and AV nodes, other parts of the conduction system, and the atrial and
ventricular muscles are shown along with the correlation to the extracellularly recorded electrical activity (ie, the electrocardiogram [ECG]). The action potentials
and ECG are plotted on the same time axis but with di erent zero points on the vertical scale. The PR interval is measured from the beginning of the P wave to the
beginning of the QRS. LAF, le anterior fascicle. (Reproduced, with permission, from Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of Medical
Physiology. 24th ed. New York: McGraw-Hill; 2012.)

Figure 4.4
A. Dissection of the cardiac action potential. Top: The action potential of a cardiac muscle fiber can be broken down into several phases: 0, depolarization; 1, initial
rapid repolarization; 2, plateau phase; 3, late rapid repolarization; 4, baseline. Bottom: Diagrammatic summary of Na+, Ca2+, and cumulative K+ currents during the
action potential. As is the convention, the inward currents are downward, and the outward currents are upward. B. Pacemaker cells in the sinoatrial (SA) node lack
the same distinct phases as the atrial and ventricular muscle cells and display prominent spontaneous diastolic depolarization.

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Phase 0 (Depolarization or Upstroke Phase)

This phase represents the depolarization phase, or the upstroke phase, similar to that of the skeletal muscle and the nerves. It is caused by the increase of the
conductance of the Na+ as a result of opening the fast Na+ channels. Once the channels open, an influx of the Na+ occurs, creating an inward Na+ current, bringing
the resting membrane toward its equilibrium potential, which is about +65 mV; however, at the peak of the upstroke, the membrane depolarizes to only about +20
mV.

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Phase 1 (Partial Repolarization)

Phase 1 is a partial repolarization at the peak of the upstroke phase, bringing the membrane potential to about 0 mV. It is caused by the outward flow of the K+
current via the transient-activated K+ channels.

Phase 2 (Plateau Phase)

Phase 2 is a long depolarization phase that has a plateau due to the balance between the inward Ca2+ current and the outward K+ current. The K+ channels that
cause the K+ e lux are called delayed rectifier potassium channels. The inward Ca2+ current is the result of opening the L-type voltage-gated Ca2+ channels (ie, L
refers to long-lasting). The Ca2+ channels open slowly and stay open for a longer period of time compared to the more e icient Na+ channels. Calcium influx during
this phase has an important role in cardiac muscle contraction by releasing Ca2+ from the sarcoplasmic reticulum (SR) via a Ca2+-induced Ca2+ release mechanism.

Phase 3 (Repolarization Phase)

Phase 3 is the repolarization phase as the voltage potential returns back to the resting membrane potential of –90 mV. The repolarization is mainly due to the K+
outward current as a result of the increased permeability to the K+ and the decreased permeability to the Ca2+.

Phase 4 (Resting Membrane Potential)

This is a stable phase when the action potential is fully repolarized and the inward and outward current are balanced. The outward K+ current is due to the high
conductance of the K+ in this phase that drives the resting membrane potential toward its equilibrium potential. The inward current is mainly due to the Na+ and
Ca2+ influx, which both have a low conductance during this phase.

The Action Potential of the SA and AV Nodes

Unlike the other cardiac cells, the action potential the SA and AV nodes is characterized by automaticity (ie, spontaneous depolarization), unstable resting
membrane potential, and the lack of the plateau phase. The SA node is the normal pacemaker of the heart; however, the AV node can take over in case of damage
to the SA node. Although the ventricle and atrial cells normally do not exhibit automaticity, in certain diseases they may, as seen in cardiac ischemia. The phases
and ionic basis of the SA and AV nodes’ action potential is shown in Fig. 4.4B and described below.

Phase 0 (Upstroke Phase)

Phase 0 in a node cell is not as rapid or sharp, and it does not reach a higher amplitude as in the other cardiac cells. It is caused by increased Ca2+ conductance that
results in an inward Ca2+ current.

Phases 1 and 2

Unlike ventricular action potential phases 1 and 2 are absent in SA and AV nodes action potential.

Phase 3 (Repolarization)

Similar to other cardiac cells, repolarization is caused by the high conductance of K+ ions that result in the K+ e lux. The large electrochemical gradient of the K+
ions drives this outward K+ current during this phase.

Phase 4 (Pacemaker Potential or Spontaneous Depolarization)

Unlike other cardiac cells, phase 4 in the nodal cells exhibits a spontaneous gradual depolarization. This property accounts for the automaticity and the ability to
spontaneously generate an action potential. The spontaneous depolarization is based on the opening of special Na+ channels that leads to an inward Na+ current If.

The “f” refers to “funny Na+ current” because these Na+ channels are unpredictable and possess unusual properties compared to the fast Na+ channels. They open
slowly and are stimulated by the preceding repolarization; the depolarization occurs gradually until it reaches a threshold where the upstroke phase starts as a
result of the T-type Ca2+ channels (ie, T refers to Transit).

The rate of depolarization in phase 4 sets up the heart rate. If the depolarization in phase 4 reaches its threshold quickly, the SA node will fire more frequently and
the heart rate will increase. The opposite is true with decreases in the heart rate as a result of the slower rate of depolarization in phase 4. The autonomic nervous
system acts on this mechanism to regulate the heart rate as discussed below.

Refractory Periods
The refractory period is when the muscle cannot respond to another stimulation. The cardiac muscle refractory period is much longer than in a skeletal muscle
because the action potential in the cardiac muscle is longer. This unique property of the cardiac muscle allows the ventricles of the heart enough time to be filled
with blood before contractions; it is also the reason that heart muscle never endures sustained contractions (ie, tetany). Fig. 4.5 shows di erent degrees of the

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refractory period during the action potential. The number of fast Na+ channels recovered and ready to respond for depolarization determines the degree of
refractory periods as follows:

The absolute refractory period (ARP) refers to the time when the cells are completely incapable of generating an action no matter how strong the stimulus. Most of
the Na+ channels are closed and cannot be opened. This includes the periods of the upstroke, plateau, and repolarization until almost –50 mV.

The e ective refractory period (ERP) extends a little more beyond the absolute refractory period where a stimulus can generate a localized action potential that
cannot be propagated.

The relative refractory period (RRP) is a period where a stronger than normal stimulus can generate an action potential. However, the characteristics of the action
potential generated in this period are abnormal, with a slower rate of rising and a shorter plateau phase. The reason for this abnormality is that some Na+ channels
have still not recovered and the K+ channels are still active.

During the supranormal period (SNP), the cardiac cell is more excitable, so a weaker than normal stimulus can generate an action potential. This is because the
membrane potential of the cell is closer to the threshold level and the majority of the Na+ channels have recovered.

Figure 4.5
Comparison of the action potentials and the contractile response of a mammalian cardiac muscle fiber in a typical ventricular cell. In the top trace, the intracellular
recording of the action potential shows the quick depolarization and extended recovery. In the bottom trace, the mechanical response is matched to the
extracellular and intracellular electrical activities. Note that in the absolute refractory period (ARP), the cardiac myocyte cannot be excited, whereas in the relative
refractory period (RRP) minimal excitation can occur. (Reproduced, with permission, from Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of
Medical Physiology. 24th ed. New York: McGraw-Hill; 2012.)

E ect of the Autonomic Nervous System on the Heart Rate and the Conduction Velocity of the Heart
The distribution of the sympathetic and parasympathetic innervations of the heart is di erent. Briefly, the parasympathetic nerves mainly supply the SA and AV
nodes and some atrial muscles, but not as much in the ventricle muscles. Sympathetic nerves, on the other hand, are equally distributed in all parts of the heart,
especially in the ventricle muscles. Normally, there is a dominant parasympathetic e ect on the SA node that sets the heart rate during rest at around 70 beats/min
instead of the intrinsic rate of 100 beats/min.

In general, the autonomic nervous system modulates the heart rate via its e ect on the SA node action potential; this is called the chronotropic e ect. Fig. 4.6
illustrates the normal rate of the SA node action potential—the sympathetic stimulation that increases the rate of the SA action potential and the heart rate (ie, a
positive chronotropic e ect) and the parasympathetic stimulation that decreases the rate of the SA action potential and the heart rate (ie, a negative chronotropic
e ect).

Figure 4.6
E ect of sympathetic (noradrenergic) and vagal (cholinergic) stimulation on the membrane potential of the SA node. Note the reduced slope of the prepotential
a er vagal stimulation and the increased spontaneous discharge a er sympathetic stimulation. (Reproduced, with permission, from Barrett KE, Barman SM,
Boitano S, Brooks HL. Ganong’s Review of Medical Physiology. 24th ed. New York: McGraw-Hill; 2012.)

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Furthermore, the autonomic nervous system changes the velocity of the action potential’s conduction through the heart and the conductive system; this is called
the dromotropic e ects. Positive dromotropic e ect means an increase in the conduction velocity, which is induced by the sympathetic nervous system. Negative
dromotropic e ect indicates a decrease in the conduction velocity, which is mediated by the parasympathetic nervous system. The mechanisms of the autonomic
nervous system e ects on both the heart rate (chronotropic) and the conduction velocity (dromotropic) are explained as follows.

Sympathetic E ect on the Heart Rate and the Conduction Velocity

Norepinephrine from the sympathetic nerve endings binds to the β1-adrenergic receptors that couple to adenyl cyclase through the Gs membrane proteins.

Activation of the β1 receptor in the SA node results in an increase of the Na+ inward current “If” and thus enhances depolarization of phase 4 (the spontaneous

depolarization phase). Furthermore, it increases the inward Ca2+ current by opening the Ca2+ channels and reducing the threshold to fire an action potential. Both
mechanisms increase the frequency of the firing action potential in the SA node and consequently increase the heart rate.

In addition, sympathetic activation increases the conduction velocity, especially in the AV node and the AV bundles. The increased permeability of the Ca2+ and the
Na+ makes it easier for the action potential to excite the next cells with shorter e ective refractory periods and thus the conduction from the atria to the ventricles is
faster.

Parasympathetic E ect on the Heart Rate and the Conduction Velocity

Acetylcholine (ACh) is released from the parasympathetic nerve endings and binds to the muscarinic (M2) receptors in the SA node that inhibit adenylyl cyclase by
coupling with Gi proteins. This inhibition of the adenylyl cyclase decreases the inward Na+ current “If” and reduces the rate of depolarization of phase 4 (the

spontaneous depolarization phase). Activation of the Gi proteins also increases the outward K+ current via the opening K+ channels, called K+-ACh, which
hyperpolarize the SA nodal membranes, making it more di icult for spontaneous depolarization. Furthermore, the inward Ca2+ current decreases with fewer Ca2+
channels, which also make di icult for the action potential to reach its threshold during phase 4 or spontaneous depolarization. All 3 of these mechanisms
contribute to a decrease in the frequency of the action potential in the SA node and decrease the heart rate with the activation of the parasympathetic nervous
system.

The parasympathetic activation (ie, vagal stimulation) decreases the conduction velocity, especially in the AV node. The mechanism of this reduction is the
hyperpolarization of the cell membranes caused by an increased outward K+ current as well as a decreased inward Ca2+ current. This results in prolonging the
e ective refractory period. The degree of reduction of the action potential traveling from the atria to the ventricle varies from mild to severe degrees, which can
lead to a complete heart block. A complete heart block means that there is no action potential passage from the atria to the ventricle, which can lead to a serious
condition that might be fatal.

Normal Electrocardiogram
Electrical currents (depolarization and repolarization) generated in the heart can be measured by an electrocardiogram (ECG). The heart’s electrical currents spread
through the tissues surrounding the heart up to the surface of the skin. The ECG uses 2 electrodes that are placed on the skin on opposite sides of the heart. The
ECG is a useful clinical diagnostic tool used to measure the electrical activity of the heart in normal and abnormal conditions, especially in: (1) rhythm disturbances
(eg, cardiac arrhythmias), (2) changes in electrical conduction (eg, heart blocks), and (3) disruption of blood supply (eg, cardiac ischemia and infarction). The details
of a normal ECG and the most common abnormalities will be discussed in this chapter. However, for the full description of an ECG and a complete description of all
the abnormalities, it is recommended that the reader refer to one of the ECG textbooks listed at the end of this chapter.

Properties of a Normal ECG

Normal ECG tracing of one heartbeat consists of a P wave, QRS complex, and T wave as illustrated in Fig. 4.7. The P wave represents the depolarization of the atrial
muscle cells which precede an atrial contraction. A er the P wave, the tracing returns to the baseline to represent the conduction of the action potential from the
atria to the ventricles. The QRS complex usually, but not always, includes 3 waves, as its name implies—the Q wave, R wave, and S wave. The QRS complex
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represents the depolarization of the ventricular muscle cells that initiates a ventricular contraction. Following the QRS complex, the tracing returns to the baseline,
representing the interval between the depolarization and the repolarization of the ventricle. The T wave represents the repolarization of the ventricular muscle
cells. Sometimes, a small deflection called a U wave, follows the T wave that is known as the late phase of ventricular depolarization.

Figure 4.7
Nomenclature of the deflections, intervals, and segments of the normal electrocardiogram. (Reproduced, with permission, from Fuster V, Walsh RA, Harrington RA,
eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011.)

Furthermore, normal ECG tracing includes the P-R interval, the ST segment, and the Q-T interval. The P-R interval represents the time between the beginning of the
P wave until the beginning of the QRS complex (ie, therefore it is sometimes called the P-Q interval, but the Q wave is o en absent). Thus, the P-R interval indicates
the duration of atrial depolarization plus the AV nodal delay, which is normally between 0.12 and 0.2 sec.

The ST segment represents the isoelectric baseline for ventricular muscle depolarization. An elevation or depression of the normal ST segment indicates an
ischemic disorder the heart.

The Q-T interval represents the duration of the action potential of the ventricular muscle cells including both depolarization and repolarization. It is measured from
the beginning of the QRS complex (it starts from the Q wave, or R wave if the Q wave is absent) to the end of the T wave. Normally, it is about 0.35 sec; however, it
ranges between 0.2 to 0.4 sec according to the heart rate. Thus, in a faster than normal heart rate, the Q-T interval will be shortened.

Recording Depolarization and Repolarization Waves in Cardiac Muscle Fibers

The action potential in cardiac muscle cells is recorded using voltmeter electrodes that are placed on the surface of the cell as shown in Fig. 4.8A. The various
phases of the action potential are recorded as follows.

At rest, the cardiac muscle cell is at a polarized state with the negative charges inside and the positive charges outside the cell membrane. A flat baseline will be
recorded if there is no electrical potential gradient or di erence between both the electrodes on the surface of the cell membrane.

During depolarization, the influx of the cations creates positive charges inside the cell and negative charges outside the cell. In partial depolarization of the cell,
when only part of the plasma membrane has negative charges outside the cell due to depolarization, while the rest of the cell membranes are still polarized with
positive charges outside the cell, an electrical potential gradient and electrical current are created that can be measured. The direction of the flow of the electrical
current is from the negative charged to positive charged. An upward deflection is recorded when the electrical current is directed toward a positive electrode. This
deflection will return to baseline when depolarization spreads to the rest of the cell membrane.

During repolarization, the e lux of the cations brings back the positive charges outside and the negative charges inside. In partial repolarization, similar to
depolarization, an electrical potential and electrical current are created, which can be detected and measured. However, in repolarization the current is moving
away from the positive electrode and thus it records as a downward deflection. Once the repolarization spreads to the rest of the plasma membrane the deflection
returns to the baseline.

Figure 4.8
A. Normal ECG. Tracings from individual electrodes (positions marked in figure) are shown for a normal ECG. B. Monophasic action potential versus ECG in
ventricular muscle. (Part A: Reproduced, with permission, from Goldman MJ. Principles of Clinical Electrocardiography. 12th ed. Originally published by Appleton &

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Lange. Copyright © 1986 by McGraw-Hill.)

ECG recordings measure the electrical currents generated in the heart, but spread and are transmitted to the skin. Thus, the voltage measured directly from the
muscle cell as in the monophasic action potential is much higher (~110 mV) than the voltage measured by the ECG (0.1 to 4 mV). A comparison between the
monophasic action potential and the ECG tracing is shown in Fig. 4.8B, which illustrates that there is no potential as recorded in the ECG when the ventricular
muscle is completely polarized or depolarized.

Direction of the Electrical Current Flow of the Heart

The action potential originating in the pacemaker of the heart spreads into the atria and then through the AV node to the septum and the rest of the ventricles. It
spreads from the endocardium to the pericardium of the heart. During partial depolarization, the outside surface of the ventricle is negatively charged while the
rest is positively charged while it is still in the polarized state. At the same time, electrical currents are generated and their direction takes on an elliptical shape
from the base to the apex of the heart, as shown in Fig. 4.9. This pattern and direction of the electrical currents occurs in almost all of the depolarization phases of
the heart, except in the very last part, the current flow reverses from the ventricular apex to the base because the last portion of the heart to be depolarized is the
other part of the ventricles near its base.

Figure 4.9
The direction of the electrical current flow in the heart.

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ECG Leads

The signal observed in an ECG recording depends on the leads used. There are 2 types of ECG leads: (1) limb (standard) leads and (2) chest leads (precordial leads).
Limb leads include (a) 3 bipolar standard limb leads and (b) 3 augmented unipolar limb leads. Thus, the all of the 12 leads of the ECG allow the recording of the
same electrical currents of the heart from 12 di erent views or angles. The limb leads refer to 6 reference axes that are representative to the body’s frontal plane,
while the chest leads demonstrate the transverse plane of the body. A brief description of each lead is provided as follows.

Three bipolar standard limb leads: In this arrangement, there are 2 electrodes placed on 2 di erent sides of the heart. One limb electrode is the positive pole and
the other single electrode is the negative reference. Normal ECG tracings for the bipolar standard limb leads are shown in Fig. 4.10.

Lead I: The negative electrode is connected to the right arm and the positive electrode is connected to the le arm.

Lead II: The negative electrode is connected to the right arm and the positive electrode is connected to the le leg.

Lead III: The negative electrode is connected to le arm and the positive electrode is connected to the le leg.

Einthoven’s law: If the electrical potentials of any 2 of the 3 bipolar limb ECG leads are known at any given instant, the third one can be calculated by summing the
first 2 leads as shown in Fig. 4.11. The positive and negative signs of those 2 leads need to be considered during summation.

Augmented unipolar limb leads: As the name implies, in this arrangement of leads there is only one positive electrode or pole attached to one limb and no single
negative pole; the other electrodes attached to the other limbs collectively form the negative pole. Normal ECG tracings for the unipolar limb leads are shown in Fig.
4.12.

aVR (augmented Voltage Right arm): The positive electrode is attached to the right arm.

aVL (augmented Voltage Le arm): The positive electrode is attached to the le arm.

aVF (augmented Voltage le Foot): The positive electrode is attached to le leg.

Figure 4.10
Three bipolar standard limb leads.

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Figure 4.11
Einthoven’s triangle.

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Figure 4.12
Augmented unipolar limb leads.

By convention, the axial reference system is established based on the aforementioned 6 limb leads as shown in Fig. 4.13. The direction from the negative electrode
to the positive electrode of each of those leads is called the axis. The axis of lead I is from the right arm to the le arm; thus, it lies in a horizontal direction and is
considered to be 0°. The rest of the axes run clockwise with an angle measured at 30° between each one; that is, +30°, +60°, +90°, and so forth. The axial system is
critical in demonstrating the direction and magnitude of the electrical activity of the heart as explained in a vectorial analysis of the ECG. A vector is an arrow that
points in the direction of the electrical potential of the heart generated by the current flow (the arrowhead points to the positive direction). The length of the arrow
is proportional to the voltage of the potential. The mean vector is an arrow directed from the base to the apex of the heart, passing through the center of the
ventricles:

Mean QRS vector = +59°


 

Figure 4.13
An axial reference system.

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Chest Leads (Precordial Leads)

To obtain a further dimension of the electrical activity of the heart, 6 chest electrodes are placed on the anterior and le lateral aspects of the chest as shown in Fig.
4.14. These are unipolar leads with positive electrodes pointing to the heart in a cross-sectional plane and recorded as V1, V2, V3, V4, V5, and V6 for normal heart
tracing. In leads V1 and V2, the QRS are recorded as downward deflections because they are located at the base of the heart where the direction of the ventricular
depolarization is traveling away from the positive electrode. However, leads V4, V5, and V6 have an upward deflection because they are located at the apex of the
heart where the depolarization waves are traveling toward the positive electrode. There are a few important common principles of ECG interpretation that can be
summarized as follows:

A depolarization wave directed toward a positive electrode results in an upward deflection on the ECG tracing of that specific lead.

A depolarization wave directed away from a positive electrode results in a downward deflection of that lead.

A repolarization wave directed toward a positive electrode results in a downward deflection of that lead.

A repolarization wave directed away from a positive electrode results in an upward deflection of that lead.

A depolarization or repolarization wave directed perpendicular to an electrode axis results in no net deflection of that lead.

Figure 4.14
Chest leads (precordial leads). (Reproduced, with permission, from Gomella LG, Haist SA. Clinician’s Pocket Reference. 11th ed. New York: McGraw-Hill; 2006.)

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Practical Interpretation of an ECG

An ECG recording appears in a standard special grid, divided in vertical and horizontal lines spaces that are 1 mm apart, as shown in Fig. 4.15. For the vertical axis,
each 1 mm equals 0.1 mV, while in the horizontal axis, each 1 mm = 0.04 sec (5 mm = 0.2 sec). To facilitate counting, every 5 mm a darker line is drawn, thus dividing
the grid into larger boxes and smaller boxes. Each large box has 5 small boxes that run vertically and horizontally.

Figure 4.15
ECG standard grid.

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It is highly recommended that a systemic approach be followed when reading any ECG tracing to avoid missing any significant information. The systemic approach
includes the following:

1. Calibration: 10 mm vertical = 1 mV

2. Rhythm: The following criteria have to be met in order to qualify the tracing as a sinus rhythm:

a. Every P wave is followed by a QRS

b. Every QRS is preceded by a P wave

c. P waves move upward in leads I, II, and III

d. A P wave interval in more than 0.12 sec (>3 small boxes)

i. Normal sinus rhythm = Heart rate between 60 and 100 beats/min and meets the above criteria

ii. Sinus bradycardia = Heart rate <60 beats/min and meet the above criteria

iii. Sinus tachycardia = Heart rate >100 beats/min and meet the above criteria

Abnormal rhythms are called arrhythmias or dysrhythmias as discussed in more detail in Chapter 9.

3. Heart rate: There are di erent methods for counting the heart rate from ECG tracings as follows (Fig. 4.16):

a. Method 1: Count the number of large boxes between the 2 adjacent R waves. Start with an R wave that aligns with a dark line of a large box. Track its next R
wave and identify the heart rate using the following sequence of numbers that you need to memorize. This method provides a quick but approximate count
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of the heart rate.

300 —150—100—75—60—50

b. Method 2: Count the number of small boxes between the 2 adjacent R waves and then use the following equation:

Heart rate = (25 mm/sec × 60 sec/min) / number of small boxes (mm) between 2 adjacent R waves= 1500 / number of small boxes (mm) between 2 adjacent R
waves

i. 25 mm/sec is the standard paper speed.

ii. This method is useful for counting a fast heart rate.

c. Method 3: Count the number of R waves within 3 seconds and multiply it by 20. Or, count the number of R waves within 6 seconds and multiply it by 10. The
marker for 3 seconds is 15 large boxes, and for 6 seconds it is 30 large boxes. This method is useful for counting an irregular heart rate.

4. Intervals

a. PR intervals: Measure from the beginning of the P wave to the beginning of the QRS complex. Normally, it measures between 0.12 to 0.2 sec (3 to 5 small
boxes). It is increased in the first-degree heart block and decreased in preexcitation syndrome and the junctional rhythm.

b. QT intervals: Measure from the start of the QRS complex until the end of the T wave. Normally, it depends on the heart rate (the faster the heart rate, the
shorter the QT interval). Thus, when it is corrected with the heart rate, the corrected QT ≤0.44 sec is normal, or visually, the QT interval is normal if it is less
than half of 2 consecutive QRS complexes. QT interval increases occur in cases of myocardial ischemia, hypocalcemia, hypokalemia, hypomagnesemia,
congenital long QT, hypothermia, acute myocardial infarction, increased intracranial pressure, and side e ects from some drugs such as antiarrhythmic
drugs. QT interval decreases occur in tachycardia and hypercalcemia.

c. QRS intervals: Measure the duration of the QRS complex that is normally ≤0.1 sec (2.5 small boxes). Increases occur in cases of bundle branch blocks,
aberrant conduction, premature ventricular contractions (PVCs) ventricular rhythms, severe hyperkalemia, and side e ects from some drugs such as
antiarrhythmic drugs.

5. Mean QRS axis/vector: The mean QRS axis is the average of the electrical currents generated during depolarization, which is directed from the base to the apex
of the heart. Normally, it ranges between –30° and +90° as shown in Fig. 4.17. If the mean QRS axis is between –30° and –90°, it indicates a le -axis deviation. If
the mean QRS axis is between +90° and +180°, it indicates a right-axis deviation. An extreme right-axis deviation or axis indeterminate (no man’s land) occurs
when the mean QRS axis is between –90° and +/–180° as shown in Fig. 4.17. There are several methods that can be used to determine the mean QRS axis. The
following are the easiest and most commonly used methods:

a. Look at the direction of QRS deflection in lead I and an aVF lead:

i. Upward deflection in both leads = Normal mean axis

ii. Upward deflection in lead I and downward in an aVF = Le -axis deviation

iii. Downward deflection in lead I and upward in an aVF = Right-axis deviation

b. A downward deflection in lead I and downward in aVF = Extreme right-axis deviation or axis indeterminate.

c. In the 6 limb leads, locate the QRS that is the most isoelectric and the mean axis will be perpendicular to that lead. Then, in that perpendicular lead if the
QRS is mainly upward, this indicates that the mean axis is directed to the positive pole; while if it is mainly downward, this indicates that the mean axis is
directed to the negative pole of that lead. This is the most commonly used method.

d. Vector analysis: This method is explained in sources referenced in the suggested readings and it is not o en used in practice.

e. A le -axis deviation results from several pathological conditions where the le ventricle thickens and hypertrophies, pushing the mean QRS axis further to
the le . These conditions include a le bundle branch block and a le anterior fascicular block. Other conditions that lead to le ventricular hypertrophy are
systemic hypertension, aortic stenosis, and some ventricular arrhythmias.

f. A right-axis deviation occurs when the mean axis is pushed further to right. This is a normal finding in infants and young adults. However, pathologically it
results from right ventricular hypertrophy that occurs due to stress on the right side of the heart such as obstructive lung disease, pulmonary hypertension,
and acute pulmonary embolism. Other conditions include a right bundle branch block, some ventricular arrhythmias, and some congenital heart diseases.

6. P wave abnormalities: Normally, the P wave represents the depolarization of the right and le atria. In the case of right atrial enlargement, the P waves are tall,
especially in leads II, III, and the aVF (P pulmonale). While with le atrial enlargement, the P waves in lead II are broad and notched (P mitrale), and in lead V1
they have deep and wide negative components. A slightly exaggerated wave can be seen, especially in lead II and lead V1.

7. QRS complex abnormalities: A normal QRS lasts for equal or less than 0.1 sec and its voltage in the limb leads ranges from 0.5 to 2.0 mV, which is measured from
the bottom of the S wave to the peak of the R wave. An abnormally high voltage occurs in ventricular hypertrophy as a result of an increase in muscle mass that

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creates more electricity. The increase in voltage di ers in di erent leads according to the site of the hypertrophy. Right ventricular hypertrophy further shi s the
mean axis to the right-axis deviation. The decrease in voltage, however, occurs in cardiac myopathies, such as in multiple old myocardial infarctions which
reduce the muscle mass and electricity. Also, fluid in the pericardial e usion causes a reduction in the electric transmission because of short-circuitry of the
electricity that results in an interruption of the electricity from the heart to the electrodes of the ECG in the skin. A similar mechanism, but to a lesser extent, is
the case of pleural e usion. Furthermore, a reduction in the cardiac action potential occurs in pulmonary emphysema due to excessive air in the lungs as well as
an enlargement of the thoracic cavity as a result of retention of air that acts as an insulator and reduces the conduction of the action potential from the heart to
the skin, which makes it di icult for the ECG leads to detect it.

A prolonged QRS complex occurs as result of a delayed or longer conduction of the depolarization of the action potential. In the case of cardiac hypertrophy or
dilatation, the depolarization takes longer than normal and the duration of the QRS can increase from 0.08 to 0.12 sec. Blocking the spread of depolarization
from the atria to the ventricle through Purkinje fibers will also prolong the QRS complex to 0.14 sec or more, depending on the severity and location of the
blockage. The pattern of a prolonged QRS can di erentiate between a right bundle branch block and a le bundle branch block, especially in chest leads, as
shown in Fig. 4.18. However, a blockage of the divisions of the le bundle branch such as a le anterior fascicular block and a le posterior fascicular block do
not prolong the QRS significantly and can be recognized in the limb leads. Furthermore, an abnormal pattern of a QRS complex also occurs due to damage of
the cardiac muscle as in the case of myocardial infarction and replacement of the cardiac tissue with fibrous tissues.

8. ST segment and T wave abnormalities: ST segment depression and/or T wave inversion is usually common in transient myocardial ischemia due to the e ect of
ischemia/reperfusion on cardiac muscle repolarization. ST segment elevations and T wave abnormalities occur in cases of acute STEMI (ST segment elevation
myocardial infarction), and its sequence of appearance as shown in Fig. 4.19, can distinguish the timing of the infarction as follows:

Initially, in the first few minutes of acute myocardial infarction there is an elevation of the ST segment, sometimes with a peak elevation of the T wave. At this
stage, a complete reperfusion and reversible cellular or tissue damage is possible with successful fibrinolytic treatment or percutaneous coronary intervention.
In this case, the ST segment will return to baseline, otherwise irreversible tissue damage will occur and the following sequence of changes will appear in the
ECG tracing.

During the first few hours, if there is no successful intervention, irreversible damage of the myocardial tissues leads to a reduction in the amplitude of the R
wave, the ST segment is still elevated and pathologic Q waves appear in certain leads based on the infarction location. Pathologic Q waves indicate a current or
previous occurrence of STEMI and usually appear in groups in various ECG leads based on the anatomic location of the infarction. The pathologic Q wave
measures more than 25% of the total QRS complex and width equal to or more than one small box. The pathologic Q wave is occurs because the necrotic tissues
do not generate or conduct the action potential.

On day 1 to day 2, the ST segment remains elevated, the T wave becomes inverted, and the pathologic Q waves deepen.

A er several days of the beginning of myocardial infarction, the ST segment returns to the baseline, the T wave remains inverted, and the pathologic Q waves
remain the same.

Weeks and months later, the ST segment remains at the baseline and the T wave returns to normal, but the pathologic Q waves persist marking the location of
the old infarction.

Figure 4.16
Measuring the heart rate from an ECG tracing (method 1 (A), method 2 (B) and methods 3 (C) as described in the text).

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Figure 4.17
The mean QRS axis and its abnormalities. (Reproduced, with permission, from Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison’s
Manual of Medicine. 19th ed. New York: McGraw-Hill; 2015.)

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Figure 4.18
QRS complex abnormalities.

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Figure 4.19
ST segment and T wave abnormalities. (Reproduced, with permission, from Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York: McGraw-
Hill; 2011.)

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The above changes in an ECG during myocardial infarction (ie, ST elevation, QRS reduction, and inverted T waves) occur in specific leads that determine its site. In
the meantime, reciprocal changes can be observed in the opposite site. The exact mechanism(s) of the changes in the ST segment during the process of myocardial
infarction is not clear, however, some theories such as diastolic current and systolic current have been used as an explanation.

Furthermore, there are many other causes that result in abnormalities of the ST segment and the T wave. For example, ST depression also occurs in acute non-ST
segment myocardial infarction, digoxin therapy, and hypokalemia.

For more detailed information on ECGs, the reader is referred to the Suggested Readings section at the end of this chapter. However, in any ECG tracings, the
following standard parameters need to be checked as these will provide critical information in assessing an individual’s heart condition:

1. Determine the heart rate: Use any of the 3 methods described earlier.

2. Assess the heart rhythm: Sinus rhythm (ie, every P wave is followed a QRS and every QRS is preceded by a P wave, a PR interval is more than 0.12 sec) or no
sinus rhythm = any type of arrhythmias.

3. Determine the intervals such as the PR interval (N = 0.12 – 0.2 sec), the QT interval (N = 0.2 – 0.4 sec or equal to or less than half the R – R interval in the case of a
normal heart rate), QRS (equal or less than 0.1 sec).

4. Mean axis (normally between -30° to +90°), beyond –30° indicates a le -axis deviation and beyond +90° indicates a right-axis deviation.

5. P wave: Check for any abnormalities such as a right or le atrial enlargement.

6. QRS complex: Check any abnormalities such as hypertrophy, bundle branch block, and myocardial infarction (a pathologic Q wave).

7. ST segment and/or T wave: Check for any abnormalities such as an ST segment elevation or depression, and a T wave inversion.

Common Cardiac Arrhythmias


A normal sinus rhythm indicates that (1) the heart rate is between 60 and 100 beats per minute, (2) the heart rate originates from the SA node, and (3) the heart rate
is conducted through the normal conductive system in the heart following the normal sequence and timing for the heart’s activation. The ECG tracing should show
that each P wave follows a QRS complex, and then a T wave is followed by a P wave again, as shown in Fig. 4.20.

Figure 4.20
Normal sinus rhythm.

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Sinus tachycardia indicates that the heart rate is more than 100 beats/min, but have otherwise normal ECG characteristics as shown in Fig. 4.21. Sinus tachycardia
occurs in several conditions, such as increased body temperature, increased sympathetic stimulation to the heart, and in thyrotoxicosis and anemia.

Figure 4.21
Sinus tachycardia.

Sinus bradycardia means that the heart rate is less than 60 beats/min, but has normal ECG characteristics as shown in Fig. 4.22. Sinus bradycardia happens in
increased vagal tone for a variety of reasons, for example, normally in young adult athletes or during sleep.

Figure 4.22
Sinus bradycardia.

Premature atrial contractions (PACs) are the result of an ectopic extra atrial contraction, not from the SA node. The additional P wave usually occurs earlier than the
sinus P wave and has an abnormal shape with di erent PR intervals as shown in Fig. 4.23. PACs sometimes occur in a normal heart or as a result of increased stress,
catecholamine, alcohol, ca eine as well as from infections, ischemia, digoxin toxicity, or atrial dilation. PACs feel like a “skipped beat” or palpitation in patients.

Figure 4.23
Premature atrial contractions.

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Atrial fibrillation: Common arrhythmias in clinical practice. Multiple atrial beats originate from ectopic foci discharging rapidly at a rate of 350 to 450 beats/min. In
ECG tracings, it looks like either small, very fast P waves or straight lines, due to the opposite direction of the waves that electrically neutralize each other. QRS
complexes are normal, but irregular in their timing as shown in Fig. 4.24. These are caused by atrial enlargement due to mitral valve diseases, coronary artery
diseases, thyrotoxicosis, cardiomyopathy, and myocarditis.

Figure 4.24
Atrial fibrillation.

Atrial flutter is an atrial ectopic foci discharge at a rate of 250 to 350 beats/min. The ECG rhythm is characterized by flutter waves (a “sawtooth” pattern) as shown in
Fig. 4.25. Only some impulses conduct through the AV node to the ventricle. The clinical consequences of atrial fibrillation and flutter occur as a result of blood
stagnation, especially in the le atrium, which leads to a predisposition of thrombus formation and consequently to a peripheral embolism and stroke. Thus, most
patients will receive anticoagulants such as warfarin or new oral anticoagulants. Furthermore, because of the lack of proper atrial systole, the diastolic filling of the
ventricle will be reduced that leads to a reduction of preload, stroke volume, and cardiac output. This will significantly worsen the condition, especially in elderly
patients with hypertension, le ventricular dysfunction, or heart failure.

Figure 4.25
Atrial flutter.

Paroxysmal supraventricular tachycardia is characterized by a sudden increase in heartbeat (150 to 250 beats/min) that originate either from the atrial or the AV
ectopic foci, and return suddenly to a normal rhythm as shown in Fig. 4.26. The most common is due to abnormal conduction in the AV node or antegrade
conduction in the accessory pathway. This occurs in young healthy individuals who grow out of it a er adolescence.

Figure 4.26
Paroxysmal supraventricular tachycardia.

Paroxysmal ventricular tachycardia originates from the ectopic ventricular foci and is characterized by sudden fast heartbeats at a rate of 150 to 250 beats/min. The
QRS complex widened with a bizarre shape, but is regular in rhythm as shown in Fig. 4.27. The P wave is usually absent, buried in the wide QRS complex. It is a
serious condition because of the severe drop in cardiac output and blood pressure, so it is most likely a result of considerable ventricular ischemia and possibly a
life-threatening condition. The cause can be from a variety of conditions, such as acute myocardial infarction, cardiomyopathy, digoxin toxicity, and congenital
heart disease.

Figure 4.27
Paroxysmal ventricular tachycardia.

Ventricular fibrillation (V fib) is the most serious of the cardiac arrhythmias; if it is not stopped within 1 to 3 minutes by electrical defibrillation, it can lead to death.
Cardiac impulses go “berserk” within the ventricle, which leads to no coordination of ventricular muscle contraction and eventually to no cardiac output and no
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tissue perfusion as shown in Fig. 4.28. It is the most common cause of sudden cardiac death. V fib is initiated by acute myocardial infarction, drug overdose,
anesthesia, cardiomyopathy, and heart trauma.

Figure 4.28
Ventricular fibrillation (V fib).

A first-degree AV block is characterized by a delay of the AV bundle conduction from the atria to the ventricle but not an actual blockage of the conduction. In the
ECG tracing, there will be a fixed prolonged P-R interval of more than 0.2 sec (N = 0.12 – 0.2) as shown in Fig. 4.29.

Figure 4.29
First-degree heart block.

A second-degree AV block is divided into 2 types: Mobitz type I (Wenckebach) and Mobitz type 2.

Mobitz type I (Wenckebach) is characterized by a progressive delay at the AV node until the impulse is completely blocked. Possible causes include an insult to the
AV node, hypoxemia, a myocardial infarction (MI), digitalis toxicity, ischemia, and increased vagal tone. This conduction does not usually progress to a higher-
degree heart block. ECG criteria include an irregular rhythm with progressive lengthening of the PR interval until there is a dropped beat (a long, longer drop). The
QRS is usually <0.12 sec as shown in Fig. 4.30A. No treatment is needed if the patient is asymptomatic.

Mobitz type 2 occurs when some impulses from the SA node fail to reach the ventricles.

Figure 4.30
A. Second-degree AV block—Mobitz type I. B. Second-degree AV Block—Mobitz type II.

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It usually occurs with acute myocardial infarction (AMI), degenerative changes in conduction, and progressive coronary artery diseases (CAD). The problem usually
occurs at the bundle of His or its branches, and may progress to a third-degree heart block. The ECG criteria include irregular rhythm (because of dropped beats),
while the PR interval remains constant until there is a block of the AV conduction, resulting in a P wave not being followed by a QRS, as shown in Fig. 4.30B.
Treatment includes (1) improving cardiac output, (2) consider temporary pacing or a permanent pacemaker, and (3) close monitoring and BP support are also
recommended.

A third-degree heart block or complete AV block is characterized by a complete block of the impulse from the atria to the ventricle as shown in Fig. 4.31. The
ventricles establish their own signal as an escape rhythm from the AV node, the AV bundle, or the ventricular tissues. The P waves become dissociated from the
QRS-T waves.

Figure 4.31
Third-degree heart block or complete AV block.

Key Points
The shape and duration of the action potential di ers in various parts of the cardiac output especially in the ventricular muscle and the pacemaker cells. These
di erences are based on the variability of the functions of those parts and are related to various ionic bases of each phase.

The hallmark of the ionic basis of the ventricular action potential is the long depolarization phase due to voltage-gated L-type Ca2+ channels. A unique feature of
the action potential of the SA node is the pacemaker potential or spontaneous depolarization due to special Na+ channels.

The long duration of the ventricular action potential results in a longer refractory period that prevents the cardiac muscle from any muscle tetanization or constant
contraction.

There is a normal precise sequence of cardiac activation and conduction that is essential for the normal sequence of cardiac muscle contraction and relaxation to
maintain normal heart function and hemodynamics.

Because the SA node, which is the natural pacemaker, has the fastest firing rate, the rest of the heart follows its lead and suppresses their own slower firing rate, a
phenomena called “overdrive suppression.” Damage to the SA node results in an ectopic pacemaker with other parts of the myocardium taking the lead.

The balance between the sympathetic and parasympathetic nervous systems has a significant e ect on heart rate, cardiac conduction and contractility at rest and
during various activities.

Normal ECG tracings record the electrical activities of the heart, representing the depolarization and repolarization of the cardiac muscle. It is a very popular and
important tool in the diagnosis for several cardiac diseases, in particular, cardiac arrhythmias, ischemia, infarction, and hypertrophy.

CLINICAL CORRELATION 4.1

Stokes-Adams syndrome: A brief fainting (ie, syncope) due to the lack of blood to the brain tissues from low cardiac output. This incidence occurs as a result of
complete block of the AV conduction which induces the ventricle to create its own impulse (ectopic pacemaker) and escape natural overdrive suppression of the SA
node. This ventricular escape allows the brain to recover from fainting and sustains its survival. Usually, these patients require an artificial pacemaker.

CLINICAL CORRELATION 4.2

The following are some useful clinical tips for diagnosing an AV block:

First-degree AV block: Prolongation of the PR interval >0.2 sec (at a rate of 70 bpm), which remains constant from beat to beat

Second-degree AV block:

Mobitz type 1:

The cycle with the dropped beat is less than 2 times the previous cycle

A shortened PR interval a er the dropped beat

The site of block is usually the AV node (proximal to the bundle of His)

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Mobitz type 2:

Fixed duration of the PR interval

A sudden appearance of blocked beats

The site of the block is infranodal

Third-degree AV block:

There is no relationship between the P waves and the QRS complexes; P waves constantly change their relationship to the QRS complexes

The ventricular rate is usually <50 bpm (may be higher in the congenital forms)

The ventricular rate is usually lower than the atrial rate

Case Studies
CASE 4.1 A 67-year-old female with a recent history of acute myocardial infarction was admitted to the emergency department because of a sudden but short
episode of unconsciousness. A er looking at her ECG, a senior resident suggests that the patient may be su ering from Stokes-Adams syndrome (a block of the
atrioventricular [AV] conductive system). If the resident’s suggestion is correct, which one of the following would be the reason for the patient’s loss of conscious?

a. Decreased total peripheral resistance (TPR)

b. Increased heart rate

c. Decreased cardiac output

d. Decreased end-diastolic volume

e. Increased blood conduction velocity

The correct answer is c.

Stokes-Adams syndrome is manifested as a brief period of loss of consciousness with or without convulsions. The cause of this syndrome is transient arrhythmias,
which result in a decrease of cardiac output. The lack of blood to the brain tissues is the reason for the loss of consciousness. The rest of the parameters in the other
answers can be secondary consequences of low cardiac output.

CASE 4.2 A 78-year-old male is brought to the emergency room (ER) by his family because he is feeling weak, a bit disoriented, and is experiencing shortness of
breath. Vital signs during physical examination show severe bradycardia and low blood pressure. His ECG tracing is shown below. Which of the following is the most
likely diagnosis?

a. Sinus bradycardia

b. First-degree heart block

c. Second-degree heart block

d. Complete heart block

e. Ventricular fibrillation

The correct answer is d.

The patient shows the typical presentation of a third-degree heart block, such as dizziness, weakness, bradycardia, and hypotension. The ECG tracing confirms the
complete heart block diagnosis, where the P waves are dissociated from the QRS waves. The other answers do not match the ECG tracing.

Suggested Readings

Dubin  D. Rapid Interpretation of EKG’s. 6th ed. Ft. Myers, FL: Cover Publishing; 2000.

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Hurst  JW. Methods used to interpret the 12-lead electrocardiogram: pattern memorization versus the use of vector concepts. Clin Cardiol. 2000;23:613.
CrossRef

Longo  DL, Fauci  AS, Kasper  DL, Hauser  SL, Jameson  JL, Loscalzo  J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York: McGraw-Hill; 2015:chaps
268, 273e.

Wagner  GS, Strauss  DG. Marriott’s Practical Electrocardiography. 12th ed. New York: Lippincott Williams & Wilkins; 2014.

Zainul  A. Essential Cardiac Electrophysiology: The Self-Assessment Approach. 2nd ed. New York: Wiley-Blackwell; 2013.

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