CHAPTER

Cardiac Conduction and

27
Rhythm Disorders
Jill M. White Winters

CARDIAC CONDUCTION SYSTEM Cardiac Conduction System

Action Potentials
Cardiac Action Potential After completing this section of the chapter, you should be able to
Absolute and Relative Refractory Periods meet the following objectives:
Electrocardiography ✦ Describe the cardiac conduction system and relate it to
DISORDERS OF CARDIAC RHYTHM the mechanical functioning of the heart
AND CONDUCTION ✦ Characterize the four phases of a cardiac action potential
Mechanisms of Arrhythmias and and differentiate between the fast and slow responses
Conduction Disorders ✦ Draw an ECG tracing and state the origin of the
Types of Arrhythmias component parts of the tracing
Sinus Node Arrhythmias ✦ Provide rationale for the importance of careful lead
Arrhythmias of Atrial Origin placement and monitoring of ischemic events
Junctional Arrhythmias
Disorders of Ventricular Conduction and Rhythm In certain areas of the heart, the myocardial cells have
Long QT Syndrome and Torsades de Pointes been modified to form the specialized cells of the conduc-
Ventricular Arrhythmias tion system. Although most myocardial cells are capable
Disorders of Atrioventricular Conduction of initiating and conducting impulses, it is the conduction
Diagnostic Methods system that maintains the pumping efficiency of the heart.
Signal-Averaged Electrocardiogram Specialized pacemaker cells generate impulses at a faster
Holter Monitoring rate than other types of heart tissue, and the conduction
Exercise Stress Testing tissue transmits these impulses at a more rapid rate than
Electrophysiologic Studies other cardiac cell types. Because of these properties, the con-
QT Dispersion duction system usually controls the rhythm of the heart.
Treatment Blood reaches the conduction tissues by way of the coro-
Pharmacologic Treatment nary blood vessels. Coronary heart disease that interrupts
Electrical Interventions blood flow through the vessels supplying tissues of the
Ablational and Surgical Interventions conduction system can induce serious and sometimes fatal
disturbances in cardiac rhythm.
The specialized excitatory and conduction system of
the heart consists of the sinoatrial (SA) node, in which the

H
eart muscle is unique among other muscles in that
it is capable of generating and rapidly conducting
its own electrical impulses or action potentials.
These action potentials result in excitation of muscle fi-
bers throughout the myocardium. Impulse formation and
conduction result in weak electrical currents that spread
through the entire body. These impulses are recorded on
an electrocardiogram. Disorders of cardiac impulse gener-
ation and conduction range from benign arrhythmias that
are merely annoying to those causing serious disruption of
heart function and sudden cardiac death.
normal rhythmic impulse is generated; the internodal
pathways between the atria and the ventricles; the atrio-
ventricular (AV) node and bundle of His, which conduct the
impulse from the atria to the ventricles; and the Purkinje
fibers, which conduct the impulses to all parts of the ven-
tricle (Fig. 27-1).
The SA node, which has the fastest intrinsic rate of fir-
ing (60 to 100 beats per minute), normally serves as the
pacemaker of the heart. It is a spindle-shaped strip of spe-
cialized muscle tissue, about 10 to 20 mm in length and 2
to 3 mm wide, located in the posterior wall of the right

581
582 UNIT VI Cardiovascular Function
Bundle of
SA node AV
His
node
A Left
B fibers
C Right bundle
branch Left bundle
branch
atrium just below of the opening of the superior vena cava
and less than 1 mm from the epicardial surface.1 Blood
supply to the SA node is provided by means of the cir-
cumflex artery. It has been suggested that no single cell in
the SA node serves as the pacemaker, but rather that sinus
nodal cells discharge synchronously because of mutual
entrainment.2 As a result, the firing of faster-discharging
cells is slowed down by slower-discharging cells, and the
firing rate of slower-discharging cells is sped up by faster-
discharging cells, resulting in a synchronization of their
firing rate.
Impulses originating in the SA node travel through
the atria to the AV node. Because of the anatomic location
of the SA node, the progression of atrial depolarization oc-
curs in an inferior, leftward, and somewhat posterior di-
rection, and the right atrium is depolarized slightly before
the left atrium.3 There are three internodal pathways be-
tween the SA node and the AV node, including the ante-
rior (Bachmann’s), middle (Wenckebach’s), and posterior
(Thorel’s) internodal tracts. These three tracts anastomose
proximal to the AV node. Interatrial conduction appears to
be accomplished through Bachmann’s bundle. This large
muscle bundle originates along the anterior border of the
SA node and travels posteriorly around the aorta to the left
atrium.4
The heart essentially has two conduction systems: one
that controls atrial activity and one that controls ventricu-
lar activity. The AV node connects the two conduction sys-
tems and provides one-way conduction between the atria
and ventricles. The AV node is a compact ovoid structure
measuring approximately 1 × 3 × 5 mm, which is located
slightly beneath the right atrial endocardium, anterior to
the opening of the coronary sinus, and immediately above
the insertion of the septal leaflet of the tricuspid valve.1,4 In
85% to 90% of people, blood supply to the AV node is pro-
vided by the right coronary artery.1 The AV node is divided
into three functional regions: the AN, or transitional, zone
between the atria and the rest of the node; the middle N,
or nodal, zone; and the NH, or upper, zone of the ventric-
Left
posterior
fascicle
anterior
fascicle
Purkinje
FIGURE 27-1 Conduction system of the heart and
action potentials. (A) Action potential of sinoatrial
(SA) and atrioventricular (AV) nodes; (B) atrial mus-
cle action potential; (C) action potential of ventric-
ular muscle and Purkinje fibers.
ular conduction system.5 Within the AN portion of the
node, atrial fibers connect with very small junctional fibers
of the node itself. The velocity of conduction through the
AN and N fibers is very slow (approximately one half that
of normal cardiac muscle), which greatly delays transmis-
sion of the impulse.5,6 A further delay occurs as the impulse
travels through the nodal region into the NH region, which
connects with the bundle of His (also called the AV bundle).
This delay provides a mechanical advantage whereby the
atria complete their ejection of blood before ventricular
contraction begins. Under normal circumstances, the AV
node provides the only connection between the atrial and
CARDIAC CONDUCTION SYSTEM
➤ The cardiac conduction system controls the rate and direc-
tion of electrical impulse conduction in the heart.
➤ Normally, impulses are generated in the SA node, which
has the fastest rate of firing, and travel via the AV node
to the Purkinje system in the ventricles.
➤ Cardiac action potentials are divided into five phases:
phase 0, or the rapid upstroke of the action potential;
phase 1, or early repolarization; phase 2, or the plateau;
phase 3, or final repolarization period; and phase 4, or
diastolic repolarization period.
➤ Cardiac muscle has two types of ion channels that function
in producing the voltage changes that occur during the de-
polarization phase of the action potential: the fast sodium
channels and the slow calcium channels.
➤ There are two types of cardiac action potentials: the fast re-
sponse, which occurs in atrial and ventricular muscle cells
and the Purkinje conduction system and uses the fast
sodium channels; and the slow response of the SA and
AV nodes, which uses the slow calcium channels.

ventricular conduction systems. The atria and ventricles
would beat independently of each other if the transmission
of impulses through the AV node were blocked.
The Purkinje system, which supplies the ventricles, has
large fibers that allow for rapid conduction and almost
simultaneous excitation of the entire right and left ventri-
cles (0.06 second).6 This rapid rate of conduction through-
out the Purkinje system is necessary for the swift and
efficient ejection of blood from the heart. The fibers of the
Purkinje system originate in the AV node and proceed to
form the bundle of His, which extends through the fibrous
tissue between the valves of the heart and into the ven-
tricular system. Because of its proximity to the aortic valve
and the mitral valve ring, the bundle of His is predisposed
to inflammation and deposits of calcified debris that can
interfere with impulse conduction.6 The bundle of His
penetrates into the ventricles and almost immediately di-
vides into right and left bundle branches that straddle the
interventricular septum. Branches from the anterior and
posterior descending coronary arteries provide blood sup-
ply for the His bundle, making this conduction site less
susceptible to ischemic damage, unless the damage is ex-
tensive.1 The bundle branches move through the sub-
endocardial tissues toward the papillary muscles and then
subdivide into the Purkinje fibers, which branch out and
supply the outer walls of the ventricles. The main trunk of
the left bundle branch extends for approximately 1 to 2 cm
before fanning out as it enters the septal area and divides
further into two segments: the left posterior and anterior fas-
cicles. The left bundle branch is supplied with blood from
both the left anterior descending artery and the posterior
descending artery (formed from the right coronary artery),
whereas the right bundle branch receives its blood from
both the right and left anterior descending coronary arte-
rial systems.1
The AV nodal fibers, when not stimulated, discharge
at an intrinsic discharge rate of 40 to 60 times a minute,
and the Purkinje fibers discharge at 15 to 40 times per
minute. Although the AV node and Purkinje system have
the ability to control the rhythm of the heart, they do not
normally do so because the discharge rate of the SA node
is considerably faster. Each time the SA node discharges,
its impulses are conducted into the AV node and Purkinje
fibers, causing them to fire. The AV node can assume the
pacemaker function of the heart should the SA node fail to
discharge, and the Purkinje system can assume the pace-
maker function of the ventricles should the AV node fail
to conduct impulses from the atria to the ventricles. Should
this occur, the heart rate will reflect the intrinsic firing rate
of these structures.
ACTION POTENTIALS
A stimulus delivered to excitable tissues (i.e., muscles,
nerves) evokes an electrical event called an action potential
(see Chapter 4). The electrical events that normally take
place in the heart are responsible for initiating each cardiac
contraction. An action potential can be divided into three
phases: the resting or unexcited state, depolarization, and
repolarization.
CHAPTER 27 Cardiac Conduction and Rhythm Disorders 583
The inside of a cardiac cell, like all living cells, contains
a negative electrical charge compared with the outside of
the cell. During the resting state, the membrane is relatively
permeable to potassium but much less so to sodium and
calcium.6 Charges of opposite polarity become aligned
along the membrane (positive on the outside and negative
on the inside; Fig. 27-2).
Depolarization occurs when the cell membrane sud-
denly becomes selectively permeable to current-carrying
ions such as sodium. Sodium ions enter the cell and result
in a sharp rise of the intracellular potential to positivity.
Repolarization involves reestablishment of the resting
membrane potential. It is a complex and somewhat slower
process, involving the outward flow of electrical charges
and the return of membrane potential to its resting state.7
During repolarization, the membrane conductance or per-
meability for potassium greatly increases, allowing the
positively charged potassium ions to move outward across
the membrane. This outward movement of potassium
removes positive charges from inside the cell; thus, the
membrane again becomes negative on the inside and pos-
itive on the outside. The sodium-potassium membrane
pump also assists in repolarization by pumping positively
charged sodium ions out across the cell membrane.8
Cardiac Action Potential
The action potential in cardiac muscle is typically divided
into five phases: phase 0—upstroke or rapid depolarization,
phase 1—early repolarization period, phase 2—plateau,
phase 3—final rapid repolarization period, and phase 4—
diastolic depolarization (Fig. 27-3). Cardiac muscle has three
types of membrane ion channels that contribute to the
voltage changes that occur during the phases of the cardiac
action potential. They are the fast sodium channels, the slow
calcium channels, and the potassium channels.
During phase 0, in atrial and ventricular muscle and in
the Purkinje system, the fast sodium channels in the cell
membrane are stimulated to open, resulting in the rapid in-
flux of sodium. The action potentials in the normal SA and
AV nodes have a much slower upstroke and are mediated
predominantly by the slow calcium currents. The point at
which the sodium gates open is called the depolarization
+++++ Resting state
– – – – –
++
– – + Depolarization
++ –
Repolarization
– –
FIGURE 27-2 The flow of charge during impulse generation in ex-
citable tissue. During the resting state, opposite charges are sepa-
rated by the cell membrane. Depolarization represents the flow of
charge across the membrane, and repolarization denotes the return
of the membrane potential to its resting state.
584 UNIT VI Cardiovascular Function
R If potassium permeability increased to its resting level at
Delay in
AV node
T to the phase 2 plateau.7 Calcium ions entering the muscle
P
Baseline
Q (several hundred milliseconds) to last 3 to 15 times longer
Depolarization S Repolarization
of atria of ventricles
Depolarization
A of ventricles
1 and the influx of calcium and sodium ceases. There is a
2 sharp rise in potassium permeability, contributing to the
3
Threshold 0 The T wave on the ECG corresponds with phase 3 of the
potential
Resting
membrane
B potential
FIGURE 27-3 Relation between (A) the electrocardiogram and
(B) phases of the ventricular action potential.
threshold. When the cell has reached this threshold, a rapid
influx of sodium occurs. The exterior of the cell now is
negatively charged in relation to the highly positive inte-
rior of the cell. This rapid influx of sodium produces a
rapid, positively directed change in the transmembrane
potential, resulting in the electrical spike and overshoot
during phase 0 of the action potential.7 The membrane
potential shifts from a resting membrane potential of ap-
proximately −90 millivolts (mV) to +20 mV (Fig. 27-4). The
rapid depolarization that constitutes phase 0 is responsi-
ble for the QRS complex on the electrocardiogram (ECG)
(see Fig. 27-3). Depolarization of a cardiac cell tends to
cause adjacent cells to depolarize because the voltage spike
of the cell’s depolarization stimulates the sodium channels
in nearby cells to open. Therefore, when a cardiac cell is
stimulated to depolarize, a wave of depolarization is prop-
agated across the heart, cell by cell.
Phase 1 occurs at the peak of the action potential and
signifies inactivation of the fast sodium channels with an
abrupt decrease in sodium permeability. The slight down-
ward slope is thought to be caused by the influx of a small
amount of negatively charged chloride ions and efflux of
potassium.1 The decrease in intracellular positivity reduces
the membrane potential to a level near 0 mV, from which
the plateau, or phase 2, arises.
Phase 2 represents the plateau of the action potential.
this time, as it does in nerve fibers or skeletal muscle, the
cell would repolarize rapidly. Instead, potassium perme-
ability is low, allowing the membrane to remain depolar-
ized throughout the phase 2 plateau. A concomitant influx
of calcium into the cell through slow channels contributes
U during this phase also play a key role in the contractile
process.1 These unique features of the phase 2 plateau in
these cells cause the action potential of cardiac muscle
than that of skeletal muscle and cause a corresponding in-
creased period of contraction.6 The phase 2 plateau coin-
cides with the ST segment of the ECG.
Phase 3 reflects final rapid repolarization and begins
with the downslope of the action potential. During the
phase 3 repolarization period, the slow channels close,
rapid outward movement of potassium and reestablish-
ment of the resting membrane potential (−90 mV). At the
conclusion of phase 3, the distribution of potassium and
sodium returns membrane to the normal resting state.
action potential.
Phase 4 represents the resting membrane potential.
4
During phase 4, the activity of the sodium-potassium pump
contributes to maintenance of the resting membrane po-
tential by transporting sodium out of the cell and moving
potassium back in. Phase 4 corresponds to diastole.
The Fast and Slow Response. There are two main types of
action potentials in the heart—the fast response and the
slow response (see Fig. 27-4). The fast response occurs in the
normal myocardial cells of the atria, the ventricles, and the
Purkinje fibers. It is characterized by the opening of voltage-
dependent sodium channels called the fast sodium channels.
The fast-response cardiac cells do not normally initiate car-
diac action potentials. Instead, impulses originating in the
specialized cells of the SA node are conducted to the fast-
response myocardial cells, where they effect a change in
membrane potential to the threshold level. On reaching
threshold, the voltage-dependent sodium channels open to
initiate the rapid upstroke of the phase 1 action potential.
The amplitude and the rate of rise of phase 1 are important
to the conduction velocity of the fast response. Myocardial
fibers with a fast response are capable of conducting electri-
cal activity at relatively rapid rates (0.5 to 5.0 m/second),
thereby providing a high safety factor for conduction.9
The slow response occurs in the SA node, which is the
natural pacemaker of the heart, and in the conduction
fibers of the AV node (see Fig. 27-4). The hallmark of these
pacemaker cells is a spontaneous phase 4 depolarization.
The membrane permeability of these cells allows a slow
inward leak of current to occur through the slow channels
during phase 4. This leak continues until the threshold for
firing is reached, at which point the cell spontaneously de-
polarizes. Under normal conditions, the slow response,
 CHAPTER 27 Cardiac Conduction and Rhythm Disorders 585

conditions. For example, such conversions may occur spon-

1
+20 taneously in individuals with severe coronary artery disease,
2 in areas of the heart where blood supply has been markedly
0 compromised or curtailed. Impulses generated by these cells
can lead to ectopic beats and serious arrhythmias.
-20 0

-40
Absolute and Relative Refractory Periods
Threshold The pumping action of the heart requires alternating con-
-60 traction and relaxation. There is a period in the action po-
3
tential curve during which no stimuli can generate another
4
-80 action potential (Fig. 27-5). This period, which is known as
the absolute refractory period, includes phases 0, 1, 2, and part
-90 of phase 3. During this time, the cell cannot depolarize
again under any circumstances. When repolarization has
Millivolts

returned the membrane potential to below threshold, al-

though not to the resting membrane potential (−90 mV),
2
+20 the cell is capable of responding to a greater-than-normal
stimulus. This condition is referred to as the relative refrac-
0 0 tory period. The relative refractory period begins when the
transmembrane potential in phase 3 reaches the threshold
-20 3 potential level and ends just before the terminal portion of
A phase 3. After the relative refractory period is a short period,
-40 called the supernormal excitatory period, during which a weak
B
stimulus can evoke a response. The supernormal excitatory
-60 period extends from the terminal portion of phase 3 until
4 the beginning of phase 4. It is during this period that cardiac
-80 arrhythmias develop.
In skeletal muscle, the refractory period is very short
-90 compared with the duration of contraction, such that a
Time (msec) second contraction can be initiated before the first is over,
resulting in a summated tetanized contraction. In cardiac
FIGURE 27-4 Changes in action potential recorded from a fast re- muscle, the absolute refractory period is almost as long
sponse in cardiac muscle cell (top) and from a slow response as the contraction, and a second contraction cannot be
recorded in the sinoatrial and atrioventricular nodes (bottom). The stimulated until the first is over. The longer length of the
phases of the action potential are identified by numbers: phase 4,
resting membrane potential; phase 0, depolarization; phase 1, brief
period of repolarization; phase 2, plateau; phase 3, repolarization.
The slow response is characterized by a slow, spontaneous rise in 1
the phase 4 membrane potential to threshold levels; it has a lesser 2
amplitude and shorter duration than the fast response. Increased
automaticity (A) occurs when the rate of phase 4 depolarization is
increased.

sometimes referred to as the calcium current, does not con- 3

tribute significantly to myocardial depolarization in the 0
atria and ventricles. Its primary role in normal atrial and
TP
ventricular cells is to provide for the entrance of calcium
for the excitation-contraction mechanism that couples the
electrical activity with muscle contraction.
The rate of pacemaker cell discharge varies with the RMP 4
resting membrane potential and the slope of phase 4 de-
polarization (see Fig. 27-4). Catecholamines (i.e., epi-
nephrine and norepinephrine) increase the heart rate by ARP RRP SN
increasing the slope or rate of phase 4 depolarization.
Acetylcholine, which is released during vagal stimulation
of the heart, slows the heart rate by decreasing the slope FIGURE 27-5 Diagram of an action potential of a ventricular muscle
of phase 4. cell, showing the threshold potential (TP), resting membrane
The fast response of atrial and ventricular muscle can potential (RMP), absolute refractory period (ARP), relative refractory
be converted to a slow pacemaker response under certain period (RRP), and supernormal (SN) period.
586 UNIT VI Cardiovascular Function

R R
1.0
mV
Delay in
AV node

0.5
PR Segment ST Segment

T T
P P
U U
Baseline 0

Q Q
PR Interval Isoelectric
Depolarization S Repolarization line
S
-0.5
of atria of ventricles QRS Duration
QT Interval
Depolarization 0 0.2 0.4 0.6
of ventricles Second

FIGURE 27-6 Diagram of the electrocardiogram (lead II) and representative depolarization and repolar-
ization of the atria and ventricle. The P wave represents atrial depolarization, the QRS complex ventric-
ular depolarization, and the T wave ventricular repolarization. Atrial repolarization occurs during
ventricular depolarization and is hidden under the QRS complex.

absolute refractory period of cardiac muscle is important
in maintaining the alternating contraction and relaxation
that is essential to the pumping action of the heart and for
the prevention of fatal arrhythmias.
ELECTROCARDIOGRAPHY
The electrocardiogram (ECG) is a graphic recording of the
electrical activity of the heart. The electrical currents gen-
erated by the heart spread through the body to the skin,
where they can be sensed by appropriately placed elec-
the recording electrode registers as a positive, or upward,
deflection. Conversely, if the impulse moves away from the
recording electrode, the deflection is downward, or nega-
tive. When there is no flow of charge between electrodes,
the potential is zero, and a straight line is recorded at the
baseline of the chart.
The ECG recorder is much like a camera in that it can
record different views of the electrical activity of the heart,
Bundle branches
Purkinje network

trodes, amplified, and viewed on an oscilloscope or chart

recorder.
His bundle

The deflection points of an ECG are designated by the

letters P, Q, R, S, and T. Figure 27-6 depicts the electrical
activity of the conduction system on an ECG tracing. The
P wave represents the SA node and atrial depolarization;
the QRS complex (i.e., beginning of the Q wave to the end AV node
of the S wave) depicts ventricular depolarization; and the
T wave portrays ventricular repolarization. The isoelectric
SA node

Atria
line between the P wave and the Q wave represents depo-
larization of the AV node, bundle branches, and Purkinje
system (Fig. 27-7). Atrial repolarization occurs during ven-
tricular depolarization and is hidden in the QRS complex. P wave ECG
The ECG records the potential difference in charge (in
QRS complex
millivolts) between two electrodes as depolarization and re-
polarization waves move through the heart and are con- FIGURE 27-7 Tissues depolarized by a wave of activation com-
ducted to the skin surface. The shape of the recorder mencing in the sinoatrial (SA) node are shown in a series of blocks
tracing is determined by the direction in which the im- superimposed on the deflections of the electrocardiogram (ECG).
pulse spreads through the heart muscle in relation to elec- (Katz A.M. [1992]. Physiology of the heart [p. 483]. New York: Raven
trode placement. A depolarization wave that moves toward Press)
 CHAPTER 27 Cardiac Conduction and Rhythm Disorders 587

depending on where the recording electrode is placed. The cardiac ECG monitoring is imperative14 (see Chapter 26).
horizontal axis of the ECG measures time (seconds), and Persons with ACS are at risk for developing extension of
the vertical axis measures the amplitude of the impulse an infarcted area, ongoing myocardial ischemia, and life-
(millivolts). Each heavy vertical line represents 0.2 second, threatening arrhythmias. Research has revealed that 80%
and each thin line represents 0.04 second (see Fig. 27-6). to 90% of ECG-detected ischemic events are clinically
The widths of ECG complexes are commonly referred to in silent.15,16 Thus, ECG monitoring is more sensitive than a
terms of duration of time. On the vertical axis, each heavy patient’s report of symptoms for identifying transient
horizontal line represents 0.5 mV. The connections of the ongoing myocardial ischemia. ECG monitoring also pro-
ECG are arranged such that an upright deflection indicates vides for more accurate and timely detection of ischemic
a positive potential and a downward deflection indicates a events, essential for treatment options such as reperfusion
negative potential. Although the vertical axis determines strategies.17 It is recommended that all 12 ECG leads be
amplitude in terms of voltage, these values frequently are used for monitoring patients with ACS because ischemic
communicated as millimeters of positive or negative de- changes that occur may be evident in different leads at dif-
flection rather than in millivolts. ferent times.
Conventionally, 12 leads (6 limb leads and 6 chest
leads) are recorded for a diagnostic ECG, each providing a
In summary, the rhythmic contraction and relaxation of the
unique view of the electrical forces of the heart from a dif-
heart rely on the specialized cells of the heart’s conduction sys-
ferent position on the body’s surface. The six limb leads
tem. Specialized cells in the SA node have the fastest inherent
view the electrical forces as they pass through the heart on
rate of impulse generation and act as the pacemaker of the
the frontal or vertical plane. The electrodes are attached to
heart. Impulses from the SA node travel through the atria to
the four extremities or representative areas on the body
the AV node and then to the AV bundle and the ventricular
near the shoulders and lower chest or abdomen. The elec-
Purkinje system. The AV node provides the only connection
trical potential recorded from any one extremity should be
between the atrial and ventricular conduction systems. The
the same no matter where the electrode is placed on the
atria and the ventricles function independently of each other
extremity. The six chest leads provide a view of the electri-
when AV node conduction is blocked.
cal forces as they pass through the heart on the horizontal
The action potential of cardiac muscle is divided into five
plane. They are moved to different positions on the chest,
phases: phase 0 represents depolarization and is characterized
including the right and left sternal borders and the left an-
by the rapid upstroke of the action potential; phase 1 is char-
terior surface. The right lower extremity lead is used as a
acterized by a brief period of repolarization; phase 2 consists
ground electrode. When indicated, additional electrodes
of a plateau, which prolongs the duration of the action poten-
may be applied to other areas of the body, such as the back
tial; phase 3 represents repolarization; and phase 4 is the rest-
or right anterior chest.
ing membrane potential. After an action potential, there is a
The goals of continuous bedside cardiac monitoring
refractory period during which the membrane is resistant to a
have shifted from simple heart rate and arrhythmia mon-
second stimulus. During the absolute refractory period, the
itoring to identification of ST-segment changes, advanced
membrane is insensitive to stimulation. This period is followed
arrhythmia identification, diagnosis, and treatment. Many
by the relative refractory period, during which a more intense
diagnostic criteria are lead specific. The monitoring leads
stimulus is needed to initiate an action potential. The relative
selected must maximize the potential for accurately iden-
refractory period is followed by a supernormal excitatory
tifying anticipated arrhythmias and ischemic events on
period, during which a weak stimulus can evoke a response.
the basis of the patient’s underlying clinical situation.
The ECG provides a means for monitoring the electrical ac-
When monitoring patients with wide QRS-complex
tivity of the heart. Conventionally, 12 leads (6 limb leads and
tachycardia (discussed later), the use of 12-lead ECG mon-
6 chest leads) are recorded for a diagnostic ECG, each provid-
itoring systems is considered optimal. For example, Drew
ing a unique view of the electrical forces of the heart from a
and Scheinman10 found that the use of 12-lead ECG mon-
different position on the body’s surface. This allows for ad-
itoring systems resulted in more than 90% accuracy when
vanced arrhythmia interpretation, detection of wide QRS-
diagnosing wide QRS arrhythmias; whereas the use of lead
complex tachycardia, and early identification of ischemic and
II, a limb lead commonly used for continuous monitoring,
infarction changes in persons with ACS.
resulted in only 34% being correctly identified.
Although accurate ECG placement and lead selection
are an important aspect of ECG monitoring, two national
surveys conducted in 1991 and 1995, respectively,11,12 iden-
tified two common errors: inaccurate electrode placement Disorders of Cardiac Rhythm
and inappropriate lead selection for individual clinical sit-
uations. Improper lead placement can significantly change and Conduction
QRS morphology, resulting in misdiagnosis of cardiac ar-
After completing this section of the chapter, you should be able to
rhythmias.13 Inappropriate lead selection can also result in
meet the following objectives:
conduction defects being missed.
In persons with acute coronary syndrome (ACS), in- ✦ Describe the possible mechanisms for arrhythmia
cluding unstable angina and ST-segment elevation and generation
non–ST-segment elevation myocardial infarction, careful ✦ Compare sinus arrhythmias with atrial arrhythmias
588 UNIT VI Cardiovascular Function
✦ Characterize the effects of atrial flutter and atrial
fibrillation on heart rhythm
✦ Describe the significance of long QT syndrome
✦ Describe the characteristics of first-, second-, and third-
degree heart block
✦ Compare the effects of premature ventricular contractions,
ventricular tachycardia, and ventricular fibrillation on
cardiac function
✦ Cite the types of cardiac conditions that can be
diagnosed using the ECG
✦ Describe the methods used in diagnosis of cardiac
arrhythmias
✦ Explain the mechanisms, criteria for use, and benefits of
antiarrhythmic drugs, internal cardioverter-defibrillator
therapy, ablation therapy, and surgical procedures in the
treatment of persons with recurrent, symptomatic
arrhythmias
There are two types of disorders of the cardiac con-
duction system: disorders of rhythm and disorders of im-
pulse conduction. The terms dysrhythmia and arrhythmia
have sometimes been used interchangeably to describe dis-
orders of cardiac rhythm. Marriott18 has pointed out that
the term arrhythmia was originally based on the usage of
the alpha privative (the prefix a-) to imply “imperfection
in” as opposed to “absence of” cardiac rhythms. However,
Marriott further pointed out that the term dysrhythmia
has not been generally accepted, and conventional use of
the term arrhythmia continues. Therefore, the term arrhyth-
mia will be used throughout this chapter.
There are many causes of cardiac arrhythmias and con-
ductions disorders, including congenital defects or degen-
erative changes in the conduction system, myocardial
ischemia and infarction, fluid and electrolyte imbalances,
and the effects of drug ingestion. Arrhythmias are not nec-
essarily pathologic; they can occur in both healthy and dis-
eased hearts. Disturbances in cardiac rhythms exert their
harmful effects by interfering with the heart’s pumping
ability. Excessively rapid heart rates (tachyarrhythmias)
reduce the diastolic filling time, causing a subsequent de-
crease in the stroke volume output and in coronary per-
fusion while increasing the myocardial oxygen needs.
Abnormally slow heart rates (bradyarrhythmias) may im-
pair the blood flow to vital organs such as the brain.
MECHANISMS OF ARRHYTHMIAS
AND CONDUCTION DISORDERS
The specialized cells in the conduction system manifest
four inherent properties that contribute to the genesis of
all cardiac rhythms, both normal and abnormal. They are
automaticity, excitability, conductivity, and refractoriness.
An alteration in any of these four properties may produce
arrhythmias or conduction defects.
The ability of certain cells in the conduction system
to initiate an impulse or action potential spontaneously is
referred to as automaticity. The SA node has an inherent
discharge rate of 60 to 100 times per minute. It normally
acts as the pacemaker of the heart because it reaches the
PHYSIOLOGIC BASIS OF ARRHYTHMIA
GENERATION
➤ Cardiac arrhythmias represent disorders of cardiac rhythm
related to alterations in automaticity, excitability, conduc-
tivity, or refractoriness of specialized cells in the conduction
system of the heart.
➤ Automaticity refers to the ability of pacemaker cells in the
heart to spontaneously generate an action potential.
Normally, the SA node is the pacemaker of the heart
because of its intrinsic automaticity.
➤ Excitability is the ability of cardiac tissue to respond to an
impulse and generate an action potential.
➤ Conductivity and refractoriness represent the ability of
cardiac tissue to conduct action potentials.
➤ Whereas conductivity relates to the ability of cardiac tissue
to conduct impulses, refractoriness represents temporary
interruptions in conductivity related to the repolarization
phase of the action potential.
threshold for excitation before other parts of the conduc-
tion system have recovered sufficiently to be depolarized.
If the SA node fires more slowly or SA node conduction is
blocked, another site that is capable of automaticity takes
over as pacemaker. Other regions that are capable of auto-
maticity include the atrial fibers that have plateau-type ac-
tion potentials, the AV node, the bundle of His, and the
bundle branch Purkinje fibers. These pacemakers have a
slower rate of discharge than the SA node. The AV node
has an inherent firing rate of 40 to 60 times per minute,
and the Purkinje system fires at a rate of 20 to 40 times per
minute. The SA node may be functioning properly, but be-
cause of additional precipitating factors, other cardiac cells
can assume accelerated properties of automaticity and
begin to initiate impulses. These additional factors might
include injury, hypoxia, electrolyte disturbances, enlarge-
ment or hypertrophy of the atria or ventricles, and expo-
sure to certain chemicals or drugs.
An ectopic pacemaker is an excitable focus outside the
normally functioning SA node. These pacemakers can re-
side in other parts of the conduction system or in muscle
cells of the atria or ventricles. A premature contraction oc-
curs when an ectopic pacemaker initiates a beat. Prema-
ture contractions do not follow the normal conduction
pathways, they are not coupled with normal mechanical
events, and they often render the heart refractory or inca-
pable of responding to the next normal impulse arising in
the SA node. They occur without incident in persons with
healthy hearts in response to sympathetic nervous system
stimulation or other stimulants such as caffeine. In the dis-
eased heart, premature contractions may lead to more se-
rious arrhythmias.
Excitability describes the ability of a cell to respond to
an impulse and generate an action potential. Myocardial
cells that have been injured or replaced by scar tissue do

not possess normal excitability. For example, during the
acute phase of an ischemic event, involved cells become
depolarized. These ischemic cells remain electrically cou-
pled to the adjacent nonischemic area; current from the
ischemic zone can induce reexcitation of cells in the non-
ischemic zone.
Conductivity is the ability to conduct impulses, and re-
fractoriness refers to the extent to which the cell is able to
respond to an incoming stimulus. The refractory period of
cardiac muscle is the interval in the repolarization period
during which an excitable cell has not recovered suffi-
ciently to be reexcited. Disturbances in conductivity or re-
fractoriness predispose to arrhythmias.
Almost all tachyarrhythmias are the result of a phe-
nomenon known as reentry.5,19–21 Under normal condi-
tions, an electrical impulse is conducted through the heart
in an orderly, sequential manner. The electrical impulse
then dies out and does not reenter adjacent tissue because
that tissue has already been depolarized and is refractory
to immediate stimulation. However, fibers that were not
activated during the initial wave of depolarization can re-
cover excitability before the initial impulse dies out, and
they may serve as a link to reexcite areas of the heart that
were just discharged and have recovered from the initial
depolarization.1,19 This activity disrupts the normal con-
duction sequence. For reentry to occur, there must be areas
of slow conduction and unidirectional conduction block
(Fig. 27-8). For previously depolarized areas to repolarize
adequately to conduct an impulse again, slow conduction
is necessary. Unidirectional block is necessary to provide a
one-way route for the original impulse to reenter, thereby
FIGURE 27-8 The role of unidirectional block in reentry. (A) An exci-
tation wave traveling down a single bundle (S) of fibers continues
down the left (L) and right (R) branches. The depolarization wave
enters the connecting branch (C) from both ends and is extin-
guished at the zone of collision. (B) The wave is blocked in the L and
R branches. (C) Bidirectional block exists in branch R. (D) The ante-
grade impulse is blocked, but the retrograde impulse is conducted
through and reenters bundle S. (Berne R.M., Levy M.N. [1988]. Phys-
iology [2nd ed., p. 417]. St. Louis: C.V. Mosby)
CHAPTER 27 Cardiac Conduction and Rhythm Disorders 589
blocking other impulses entering from the opposite direc-
tion from extinguishing the reentrant circuit. Reentry re-
quires a triggering stimulus such as an extrasystole. If
sufficient time has elapsed for the refractory period in the
reentered area to end, a self-perpetuating, circuitous move-
ment can be initiated.1
Reentry may occur anywhere in the conduction system.
The functional components of a reentry circuit can be large
and include an entire specialized conduction system, or the
circuit can be microscopic. It can include myocardial tissue,
AV nodal cells, junctional tissue, or the ventricles. Factors
contributing to the development of a reentrant circuit in-
clude ischemia, infarction, and elevated serum potassium
levels.22 Scar tissue interrupts the normally low-resistance
paths between viable myocardial cells, slowing conduction,
promoting asynchronous myocardial activation, and pre-
disposing to unidirectional conduction block. Specially fil-
tered signal-averaged electrocardiography can be used to
detect the resultant late potentials. Effects of drugs such
as epinephrine can produce a shortened refractory period,
thereby increasing the likelihood of reentrant arrhythmias.
There are several forms of reentry. The first is anatomic
reentry. It consists of an excitation wave that travels in a
set pathway.1,23 Arrhythmias that arise as a result of ana-
tomic reentry are paroxysmal supraventricular tachycar-
dias, as seen in Wolff-Parkinson-White syndrome, atrial
fibrillation, atrial flutter, AV nodal reentry, and some ven-
tricular tachycardias. Functional reentry does not rely on
an anatomic structure to circle; rather, it depends on the
local differences in conduction velocity.1,23 Spiral reentry is
the most common form of this type of reentry.24 It is initi-
ated by a wave of electrical current that does not propagate
naturally in its normal plane after meeting refractory tis-
sue. The broken end of the wave curls, forms a vortex, and
permanently rotates. This phenomenon suppresses normal
pacemaker activity and can result in atrial fibrillation.23 Ar-
rhythmias observed with functional reentry are likely to be
polymorphic because of charging circuits.1 Reflection is
sometimes considered another form of reentry that can
occur in parallel pathways of myocardial tissue or the Purk-
inje network. With reflection, the cardiac impulse reaches
the depressed segment, triggers the surrounding tissue, and
then returns in a retrograde direction through the severely
depressed region. Reflection differs from true reentry in
that the impulse travels along the same pathway in both
directions and does not require a circuit.1
TYPES OF ARRHYTHMIAS
Sinus Node Arrhythmias
In a healthy heart driven by sinus node discharge, the
heart rate ranges between 60 and 100 beats per minute. On
the ECG, a P wave may be observed to precede every QRS
complex. Historically, normal sinus rhythm has been con-
sidered the “normal” rhythm of a healthy heart. In normal
sinus rhythm, a P wave precedes each QRS complex, and
the RR intervals, which are used to measue heart rate, re-
main relatively constant over time (Fig. 27-9). Alterations
in the function of the SA node lead to changes in rate or
rhythm of the heartbeat.
590 UNIT VI Cardiovascular Function
D ening and shortening of RR intervals.
Years ago, it was believed that sinus rhythm should be
regular; that is, all RR intervals should be equal. Today, it
is accepted that a more optimal rhythm is respiratory
sinus arrhythmia. Respiratory sinus arrhythmia is a cardiac
rhythm characterized by gradual lengthening and shorten-
ing of RR intervals (see Fig. 27-9). This variation in cardiac
cycles is related to intrathoracic pressure changes that occur
with respiration and resultant alterations in autonomic
control of the SA node. Inspiration causes acceleration of
the heart rate, and expiration causes slowing. Respiratory
sinus arrhythmia accounts for most heart rate variability in
healthy individuals. Decreased heart rate variability has
been associated with altered health states, including myo-
cardial infarction, congestive heart failure, hypertension,
diabetes mellitus, and prematurity in infants.
Sinus Bradycardia. Sinus bradycardia describes a slow
(<60 beats per minute) heart rate (see Fig. 27-9). In sinus
bradycardia, a P wave precedes each QRS. A normal P wave
and PR interval (0.12 to 0.20 second) indicate that the im-
pulse originated in the SA node rather than in another area
of the conduction system that has a slower inherent rate.
Vagal stimulation decreases the firing rate of the SA node
and conduction through the AV node to cause a decrease
in heart rate. This rhythm may be normal in trained ath-
letes, who maintain a large stroke volume, and during
sleep. Sinus bradycardia may be an indicator of poor prog-
nosis when it occurs in conjunction with acute myocardial
infarction, particularly if associated with hypotension.
FIGURE 27-9 Electrocardiographic (ECG) tracings of rhythms
originating in the sinus node. (A) Normal sinus rhythm (60 to
100 beats per minute). (B) Sinus bradycardia (<60 beats per
minute). (C) Sinus tachycardia (>100 beats per minute). (D) Res-
piratory sinus arrhythmia, characterized by gradually length-
Sinus Tachycardia. Sinus tachycardia refers to a rapid
heart rate (>100 beats per minute) that has its origin in the
SA node (see Fig. 27-9). A normal P wave and PR interval
should precede each QRS complex. The mechanism of
sinus tachycardia is enhanced automaticity related to sym-
pathetic stimulation or withdrawal of vagal tone. Sinus
tachycardia is a normal response during fever and exercise
and in situations that incite sympathetic stimulation. It
may be associated with congestive heart failure, myocardial
infarction, and hyperthyroidism. Pharmacologic agents
such as atropine, isoproterenol, epinephrine, and quinidine
also can cause sinus tachycardia.
Sinus Arrest. Sinus arrest refers to failure of the SA node to
discharge and results in an irregular pulse. An escape rhythm
develops as another pacemaker takes over. Sinus arrest
may result in prolonged periods of asystole and often pre-
disposes to other arrhythmias. Causes of sinus arrest in-
clude disease of the SA node, digitalis toxicity, myocardial
infarction, acute myocarditis, excessive vagal tone, quini-
dine, acetylcholine, and hyperkalemia or hypokalemia.25
Sick Sinus Syndrome. Sick sinus syndrome is a term that
describes a number of forms of cardiac impulse formation
and intra-atrial and AV conduction abnormalities.26–28 The
syndrome most frequently is the result of total or subtotal
destruction of the SA node, areas of nodal–atrial disconti-
nuity, inflammatory or degenerative changes of the nerves
and ganglia surrounding the node, or pathologic changes
 CHAPTER 27 Cardiac Conduction and Rhythm Disorders 591

in the atrial wall.28 In addition, occlusion of the sinus node supraventricular tachycardia, atrial flutter, and atrial fibril-
artery may be a significant contributing factor. Approxi- lation (Fig. 27-10).
mately 40% of adults with sick sinus syndrome also have
Premature Atrial Contractions. Premature atrial contrac-
coronary heart disease.29 In children, the syndrome is most
tions (PACs) are contractions that originate in the atrial
commonly associated with congenital heart defects, par-
conduction pathways or atrial muscle cells and occur be-
ticularly following corrective cardiac surgery.28
fore the next expected SA node impulse. This impulse to
The arrhythmias associated with sick sinus syndrome
contract usually is transmitted to the ventricle and back to
include spontaneous persistent sinus bradycardia that is not
the SA node. The location of the ectopic focus determines
drug induced or appropriate for the physiologic circum-
the configuration of the P wave. In general, the closer the
stances, prolonged sinus pauses, combinations of SA and
ectopic focus is to the SA node, the more the ectopic com-
AV node conduction disturbances, or alternating parox-
plex resembles a normal sinus complex. The retrograde
ysms of rapid regular or irregular atrial tachyarrhythmias
transmission to the SA node often interrupts the timing of
and periods of slow atrial and ventricular rates (bradycardia-
the next sinus beat, such that a pause occurs between the
tachycardia syndrome).30 Most commonly, the term sick si-
two normally conducted beats. In healthy individuals,
nus syndrome is used to refer to the bradycardia-tachycardia
PACs may be the result of stress, tobacco, or caffeine. They
syndrome. The bradycardia is caused by disease of the sinus
also have been associated with myocardial infarction, dig-
node (or other intraatrial conduction pathways), and the
italis toxicity, low serum potassium or magnesium levels,
tachycardia is caused by paroxysmal atrial or junctional ar-
and hypoxia.
rhythmias. Individuals with this syndrome often are asymp-
tomatic. Ironically, the development of atrial fibrillation Paroxysmal Supraventricular Tachycardia. Paroxysmal
may alleviate symptoms in persons who are symptomatic supraventricular tachycardia is sometimes referred to
because heart rate can be controlled more consistently as paroxysmal atrial tachycardia. This term includes all
under these circumstances.27
The most common manifestations of sick sinus syn-
drome are lightheadedness, dizziness, and syncope, symp-
QRS QRS QRS
toms related to the bradyarrhythmias.29,31 When patients
with sick sinus syndrome experience palpitations, they are Atrial
PP PPPPPP P P
generally the result of tachyarrhythmias and are suggestive flutter
of the presence of bradycardia-tachycardia syndrome.29
Treatment depends on the rhythm problem and fre-
quently involves the implantation of a permanent pace-
maker. Pacing for the bradycardia, combined with drug Atrial
therapy to treat the tachycardia, is often required in brady- fibrillation
cardia-tachycardia syndrome.28 Medications that affect SA
node discharge must be cautiously used.
Fibrillatory P waves

Arrhythmias of Atrial Origin

Impulses from the SA node pass through the conductive Paroxysmal
pathways in the atria to the AV node. Arrhythmias of atrial atrial QRS QRS QRS QRS QRS QRS
origin include premature atrial contractions, paroxysmal tachycardia
P T P T P T P TP TP TP
(PAT)

Normal sinus rhythm Onset PAT

SUPRAVENTRICULAR AND VENTRICULAR
ARRHYTHMIAS
➤ Supraventricular arrhythmias represent disorders of atrial
rhythm or conduction.
➤ Atrioventricular nodal and junctional arrhythmias result
from disruption in conduction of impulses from the atria to
the ventricles.
➤ Ventricular arrhythmias represent disorders of ventricular
rhythm or conduction.
➤ Because the ventricles are pumping chambers of the heart,
arrhythmias that produce an abnormally slow (e.g.,heart
block) or rapid ventricular rate (e.g., ventricular tachycardia
or fibrillation) are potentially life threatening.
Premature PAC
atrial QRS QRS QRS
contractions
(PAC)
FIGURE 27-10 Electrocardiographic tracings of atrial arrhythmias.
Atrial flutter (first tracing) is characterized by the atrial flutter (F) waves
occurring at a rate of 240 to 450 beats per minute. The ventricular
rate remains regular because of the conduction of every sixth atrial
contraction. Atrial fibrillation (second tracing) has grossly disorga-
nized atrial electrical activity that is irregular with respect to rate and
rhythm. The ventricular response is irregular, and no distinct P waves
are visible. The third tracing illustrates paroxysmal atrial tachycardia
(PAT), preceded by a normal sinus rhythm. The fourth tracing illus-
trates premature atrial complexes (PAC).
592 UNIT VI Cardiovascular Function
tachyarrhythmias that originate above the bifurcation of
the bundle of His and have a sudden onset and termina-
tion. They may be the result of AV nodal reentry, Wolff-
Parkinson-White syndrome (caused by an accessory
conduction pathway between the atria and ventricles), or
intraatrial or sinus node reentry. Paroxysmal supraven-
tricular tachycardias tend to be recurrent and of short
duration.
Atrial Flutter. Atrial flutter is a rapid atrial ectopic tachy-
cardia, with an atrial rate that ranges from 240 to 450 beats
per minute. There are two types of atrial flutter.27 Type I
flutter (classic) is the result of a reentry mechanism in the
right atrium and can be entrained and interrupted with
atrial pacing techniques. The atrial rate in typical type I
flutter usually is in the vicinity of 300 beats per minute,
but it can range from 240 to 340 beats per minute. The
mechanism of type II flutter is unknown. With type II flut-
ter, the atrial rate ranges from 350 to 450 beats per minute.
On the ECG, atrial flutter generates a defined sawtooth
pattern in leads II, III, aVF, and V1.32 The ventricular re-
sponse rate and regularity are variable and depend on the
AV conduction sequence. When regular, the ventricular
response rate usually is a defined fraction of the atrial rate
(i.e., when conduction from the atria to the ventricles is
2⬊1, an atrial flutter rate of 300 would result in a ventricu-
lar response rate of 150 beats per minute). The QRS complex
may be normal or abnormal, depending on the presence or
absence of preexisting intraventricular conduction defects
or aberrant ventricular conduction.
Atrial flutter rarely is seen in normal, healthy individ-
uals. It may be seen in persons of any age in the presence
of underlying atrial abnormalities. Subgroups that are at
particularly high risk for development of atrial flutter in-
clude children, adolescents, and young adults who have
undergone corrective surgery for complex congenital heart
diseases.27
Atrial Fibrillation. Atrial fibrillation is characterized by
chaotic impulses propagating in different directions and
causing disorganized atrial depolarizations without effec-
tive atrial contraction.33 In most cases, multiple, small re-
entrant circuits are constantly arising in the atria, colliding,
being extinguished, and arising again. Fibrillation occurs
when the atrial cells cannot repolarize in time for the next
incoming stimulus. Atrial fibrillation is characterized on
the ECG by a grossly disorganized pattern of atrial electri-
cal activity that is irregular with respect to rate and rhythm
and the absence of discernible P waves. Atrial activity is de-
picted by fibrillatory (f) waves of varying amplitude, dura-
tion, and morphology. These f waves appear as random
oscillation of the baseline. Because of the random con-
duction through the AV node, QRS complexes appear in
an irregular pattern.
Atrial fibrillation is the only common arrhythmia in
which the ventricular rate is rapid and the rhythm irregu-
lar.34 The atrial rate typically ranges from 400 to 600 beats
per minute, with many impulses blocked at the AV node.
The ventricular response is completely irregular, ranging
from 80 to 180 beats per minute in the untreated state. Be-
cause of changes in stroke volumes resulting from varying
periods of diastolic filling, not all ventricular beats pro-
duce a palpable pulse. The difference between the apical
rate and the palpable peripheral pulses is called the pulse
deficit. The pulse deficit may increase when the ventricu-
lar rate is high.
Atrial fibrillation may appear paroxysmally or as a
chronic phenomenon.31 It can be seen in persons without
any apparent disease, or it may occur in individuals with
coronary artery disease, mitral valve disease, ischemic heart
disease, hypertension, myocardial infarction, pericarditis,
congestive heart failure, digitalis toxicity, and hyperthy-
roidism. Spontaneous conversion to sinus rhythm within
24 hours of atrial fibrillation is common, occurring in up to
two thirds of persons with the disorder.33 Once the duration
exceeds 24 hours, the likelihood of conversion decreases,
and after 1 week of persistent arrhythmia, spontaneous con-
version is rare.33
Atrial fibrillation is the most common chronic ar-
rhythmia with an incidence and prevalence that increases
with age. The incidence of chronic atrial fibrillation dou-
bles with each decade of life and ranges from 2 or 3 new
cases per 1000 population per year between the ages of 55
and 64 years, to 35 new cases per 1000 per year between
the ages of 85 and 95 years.33
The symptoms of chronic atrial fibrillation vary. Some
people have minimal symptoms, and others have severe
symptoms, particularly at the onset of the arrhythmia.
The symptoms may range from palpitations to acute pul-
monary edema. Fatigue and other nonspecific symptoms
are common in the elderly. The condition predisposes
individuals to thrombus formation in the atria, with sub-
sequent risk for embolic stroke.
The treatment of atrial fibrillation is dependent on its
cause, recency of onset, and persistence of the arrhythmia.
Anticoagulant medications may be used to prevent em-
bolic stroke, and medications (e.g., digitalis, beta blockers)
may be used to control the ventricular rate in persons with
persistent atrial fibrillation.33,34 Cardioversion may be con-
sidered in some persons, particularly those with pulmonary
edema or unstable cardiac status. Because conversion to
sinus rhythm is associated with increased risk for thrombo-
embolism, anticoagulation therapy is usually administered
for at least 3 weeks before cardioversion is attempted in per-
sons in whom the duration of atrial fibrillation is unknown
or exceeds 2 to 3 days.33 Transesophageal echocardiography
can be used to detect atrial thrombus, and transesophageal
echo-guided cardioversion provides a means of ensuring
that atrial thrombus is not present when cardioversion is
attempted. Anticoagulant medication is usually continued
after cardioversion.
Junctional Arrhythmias
The AV node can act as a pacemaker in the event the SA
node fails to initiate an impulse. Junctional rhythms can
be transient or permanent, and they usually have a rate of
40 to 60 beats per minute. Junctional fibers in the AV
node or bundle of His also can serve as ectopic pacemak-
ers, producing premature junctional complexes. Another
rhythm originating in the junctional tissues is nonparox-
ysmal junctional tachycardia. This rhythm usually is of

gradual onset and termination. However, it may occur
abruptly if the dominant pacemaker slows sufficiently.
The rate associated with junctional tachycardia ranges
from 70 to 130 beats per minute, but it may be faster.1 The
P waves may precede, be buried in, or follow the QRS
complexes, depending on the site of the originating im-
pulses. The clinical significance of nonparoxysmal junc-
tional tachycardia is the same as for atrial tachycardias.
Catheter ablation therapy has been used successfully to
treat some individuals with recurrent or intractable junc-
tional tachycardia. Nonparoxysmal junctional tachycardia
is observed most frequently in individuals with underlying
heart disease, such as inferior wall myocardial infarction
or myocarditis, or after open-heart surgery. It also may be
present in persons with digitalis toxicity.
Disorders of Ventricular Conduction
and Rhythm
The junctional fibers in the AV node join with the bundle
of His, which divides to form the right and left bundle
branches. The bundle branches continue to divide and form
the Purkinje fibers, which supply the walls of the ventricles
(see Fig. 27-1). As the cardiac impulse leaves the junctional
fibers, it travels through the AV bundle. Next, the impulse
moves down the right and left bundle branches that lie be-
neath the endocardium on either side of the septum. It then
spreads out through the walls of the ventricles. Interruption
of impulse conduction through the bundle branches is
called bundle branch block. These blocks usually do not cause
alterations in the rhythm of the heartbeat. Instead, a bun-
dle branch block interrupts the normal progression of de-
polarization, causing the ventricles to depolarize one after
the other because the impulses must travel through muscle
tissue rather than through the specialized conduction tis-
sue.35 This prolonged conduction causes the QRS complex
to be wider than the normal 0.04 to 0.10 second. The left
bundle branch bifurcates into the left anterior and posterior
fascicles. An interruption of one of these fascicles is referred
to as a hemiblock.
Long QT Syndrome and Torsades de Pointes
The long QT syndrome (LQTS) is characterized by prolon-
gation of the QT interval that may result in a characteris-
tic type of polymorphic ventricular tachycardia called
torsades de pointes and sudden cardiac death.36–38 Torsades
de pointes (twisting or rotating around a point) is a spe-
cific type of ventricular tachycardia (Fig. 27-11). The term
refers to the polarity of the QRS complex, which swings
from positive to negative and vice versa. The QRS ab-
normality is characterized by large, bizarre, polymorphic,
FIGURE 27-11 Torsades de pointes. (From Hudak C.M., Gallo B.M.,
Morton P.G. (1998). Critical care nursing: A holistic approach [7th ed.,
p. 216]. Philadelphia: Lippincott-Raven)
CHAPTER 27 Cardiac Conduction and Rhythm Disorders 593
multiformed QRS complexes that vary, often from beat to
beat, in amplitude and direction, at, as well as in, rotation
of the complexes around the isoelectric line. The rate of
tachycardia is 100 to 180 beats per minute but can be as
fast as 200 to 300 beats per minute. The rhythm is highly
unstable and may terminate in ventricular fibrillation or
revert to sinus rhythm.
LQTS is caused by various agents and conditions that
reduce the magnitude of outward repolarizing potassium
currents, enhance the magnitude of the inward depolariz-
ing sodium and calcium currents, or both. Thus, there is
delayed repolarization of the ventricles with development
of early depolarizing afterpotentials that initiate the ar-
rhythmia. Typically, the QT interval is measured in a lead
in which the T wave is prominent and its end is easily dis-
tinguished, such as V2 or V3. Because the QT interval short-
ens with tachycardia and lengthens with bradycardia, it is
typically corrected for heart rate and is noted as QTc.39–42
Nonetheless, a QTc greater than 440 msec in men and
greater than 460 msec in women has been linked with
episodes of sudden arrhythmia death syndrome. In addi-
tion, T-wave morphology frequently is abnormal in patients
with LQTS.1,43
LQTS has been classified into hereditary and acquired
forms, both of which are associated with the development
of torsades de pointes and sudden cardiac death. The
hereditary forms of LQTS are caused by disorders of mem-
brane ion-channel proteins, with either potassium chan-
nel defects or sodium channel defects.1 In some cases, the
disorder may result from a gene defect that alters the func-
tion of a single ion channel. The gene mutations that
result in congenital LQTS have been identified on chro-
mosomes 3, 4, 7, 11, and 21.44 The hereditary forms of
LQTS are typically considered adrenergic dependent be-
cause they are generally triggered by increased activity of
the sympathetic nervous system.36
Acquired LQTS has been linked to a variety of condi-
tions, including cocaine use, exposure to organophospho-
rous compounds, electrolyte imbalances, marked brady-
cardia, myocardial infarction, subarachnoid hemorrhage,
autonomic neuropathy, human immunodeficiency virus
HIV infection, and protein-sparing fasting.36,37,38,45 Med-
ications linked to LQTS include digitalis, antiarrhythmic
agents (e.g., amiodarone, procainamide, and quinidine),
verapamil (calcium channel blocker), haloperidol (anti-
psychotic agent), and erythromycin (antibiotic).37 The
acquired forms of LQTS are often classified as pause de-
pendent because the torsades associated with them gener-
ally occurs at slow heart rates or in response to short-long-
short RR-interval sequences. Treatment of acquired forms
of LQTS is primarily directed at identifying and withdraw-
ing the offending agent, although emergency-type mea-
sures that modulate the function of transmembrane ion
currents can be lifesaving.
Ventricular Arrhythmias
Arrhythmias that arise in the ventricles commonly are
considered more serious than those that arise in the atria
because they afford the potential for interfering with the
pumping action of the heart.
594 UNIT VI Cardiovascular Function
Premature Ventricular Contractions. A premature ven-
tricular contraction (PVC) is caused by a ventricular ectopic
pacemaker. After a PVC, the ventricle usually is unable to
repolarize sufficiently to respond to the next impulse that
arises in the SA node. This delay is commonly referred to as
a compensatory pause, which occurs while the ventricle
waits to reestablish its previous rhythm (Fig. 27-12). When
a PVC occurs, the diastolic volume usually is insufficient
for ejection of blood into the arterial system. As a result,
PVCs usually do not produce a palpable pulse, or the pulse
amplitude is significantly diminished. In the absence of
heart disease, PVCs typically are not clinically significant.
The incidence of PVCs is greatest with ischemia, acute
myocardial infarction, history of myocardial infarction,
ventricular hypertrophy, infection, increased sympathetic
nervous system activity, or increased heart rate.46 PVCs also
can be the result of electrolyte disturbances or medications.
A special pattern of PVC called ventricular bigeminy is a
condition in which each normal beat is followed by or
paired with a PVC. This pattern often is an indication of
digitalis toxicity or heart disease. The occurrence of fre-
quent PVCs in the diseased heart predisposes the patient to
the development of other, more serious arrhythmias, in-
cluding ventricular tachycardia and ventricular fibrillation.
Ventricular Tachycardia. Ventricular tachycardia describes
a cardiac rhythm originating distal to the bifurcation of
the bundle of His, in the specialized conduction system in
ventricular muscle, or both.1 It is characterized by a ven-
PVC PVC
Premature
ventricular Normal beats
contractions
(PVC)
Ventricular
tachycardia
Ventricular
fibrillation
FIGURE 27-12 Electrocardiographic (ECG) tracings of ventricular ar-
rhythmias. Premature ventricular contractions (PVCs) (top tracing)
originate from an ectopic focus in the ventricles, causing a distor-
tion of the QRS complex. Because the ventricle usually cannot re-
polarize sufficiently to respond to the next impulse that arises in the
sinoatrial node, a PVC frequently is followed by a compensatory
pause. Ventricular tachycardia (middle tracing) is characterized by a
rapid ventricular rate of 70 to 250 beats per minute and the ab-
sence of P waves. In ventricular fibrillation (bottom tracing), there are
no regular or effective ventricular contractions, and the ECG tracing
is totally disorganized.
tricular rate of 70 to 250 beats per minute, and the onset
can be sudden or insidious. Usually, ventricular tachy-
cardia is exhibited electrocardiographically by wide, tall,
bizarre-looking QRS complexes that persist longer than
0.10 second (see Fig. 27-12). QRS complexes can be uniform
in appearance, or they can vary randomly, in a repetitive
manner (e.g., torsades de pointes), in an alternating pat-
tern (e.g., bidirectional), or in a stable but changing fash-
ion. Ventricular tachycardia can be sustained, lasting more
than 30 seconds and requiring intervention, or it can be
nonsustained and stop spontaneously. This rhythm is dan-
gerous because it eliminates atrial kick and can cause a
reduction in diastolic filling time to the point at which car-
diac output is severely diminished or nonexistent.
Ventricular Flutter and Fibrillation. These arrhythmias
represent severe derangements of cardiac rhythm that ter-
minate fatally within minutes unless corrective measures
are taken promptly. The ECG pattern in ventricular flutter
has a sine wave appearance with large oscillations occur-
ring at a rate of 150 to 300 per minute.38 In ventricular fib-
rillation, the ventricle quivers but does not contract. The
classic ECG pattern of ventricular fibrillation is that of
gross disorganization without identifiable waveforms or
intervals (see Fig. 27-12). When the ventricles do not con-
tract, there is no cardiac output, and there are no palpable
or audible pulses. The immediate defibrillation using a
nonsynchronized DC electrical shock is mandatory for
ventricular fibrillation and for ventricular flutter that has
caused loss of consciousness.28
Disorders of Atrioventricular Conduction
Under normal conditions, the AV junction, which consists
of the AV node with its connections to the entering atrial
internodal pathways, the AV bundle, and the nonbranch-
ing portion of the bundle of His, provides the only con-
nection for transmission of impulses between the atrial
and ventricular conduction systems. Junctional fibers in
the AV node have high-resistance characteristics that cause
a delay in the transmission of impulses from the atria to
the ventricles. This delay provides optimal timing for atrial
contribution to ventricular filling and protects the ventri-
cles from abnormally rapid rates that arise in the atria.
Conduction defects of the AV node are most commonly
associated with fibrosis or scar tissue in fibers of the con-
duction system. Conduction defects also may result from
medications, including digoxin, β-adrenergic–blocking
agents, calcium channel–blocking agents, and class 1A
antiarrhythmic agents.47 Additional contributing factors
include electrolyte imbalances, inflammatory disease, or
cardiac surgery.
Heart block refers to abnormalities of impulse con-
duction. It may be normal, physiologic (e.g., vagal tone),
or pathologic. It may occur in the AV nodal fibers or in the
AV bundle (i.e., bundle of His), which is continuous with
the Purkinje conduction system that supplies the ventri-
cles. The PR interval on the ECG corresponds with the
time it takes for the cardiac impulse to travel from the SA
node to the ventricular pathways. Normally, the PR inter-
val ranges from 0.12 to 0.20 second.

First-Degree AV Block. First-degree AV block is character-
ized by a prolonged PR interval (exceeds 0.20 second)
(Fig. 27-13). The prolonged PR interval indicates delayed
AV conduction, but all atrial impulses are conducted to the
ventricles. This condition usually produces a regular atrial
and ventricular rhythm. Clinically significant PR interval
prolongation can result from conduction delays in the AV
node itself, the His-Purkinje system, or both.1 When the
QRS complex is normal in contour and duration, the AV
delay almost always occurs in the AV node and rarely in
the bundle of His. In contrast, when the QRS complex is
prolonged, showing a bundle branch block pattern, con-
duction delays may be in the AV node or the His-Purkinje
system. First-degree block may be the result of disease in
the AV node such as ischemia or infarction, or of infec-
tions such as rheumatic fever or myocarditis.48–50 Isolated
first-degree heart block usually is not symptomatic, and
temporary or permanent cardiac pacing is not indicated.
Second-Degree AV Block. Second-degree AV block is char-
acterized by intermittent failure of conduction of one or
more impulses from the atria to the ventricles. The non-
conducted P wave can appear intermittently or frequently.
A distinguishing feature of second-degree AV block is that
conducted P waves relate to QRS complexes with recurring
PR intervals; that is, the association of P waves with QRS
complexes is not random.1 Second-degree AV block has
been divided into two types: type I (i.e., Mobitz type I or
Wenckebach’s phenomenon) and type II (i.e., Mobitz
type II). A Mobitz type I AV block is characterized by pro-
AV block
1st degree
PR= 0.38 sec.
QRS QRS QRS
AV block
T P
2nd degree P P T P P DIAGNOSTIC METHODS
QRS QRS QRS
AV block
P PT P P P PT P P TP
3rd degree
FIGURE 27-13 Electrocardiographic changes that occur with alter-
ations in atrioventricular (AV) node conduction. The top tracing
shows the prolongation of the PR interval, which is characteristic of
first-degree AV block. The middle tracing illustrates Mobitz type II
second-degree AV block, in which the conduction of one or more
P waves is blocked. In third-degree AV block (bottom tracing), com-
plete block in conduction of impulses through the AV node occurs,
and the atria and ventricles develop their own rates of impulse
generation.
CHAPTER 27 Cardiac Conduction and Rhythm Disorders 595
gressive lengthening of the PR interval until an impulse is
blocked and the sequence begins again. It frequently occurs
in persons with inferior wall myocardial infarction, partic-
ularly with concomitant right ventricular infarction.1 The
condition usually is associated with an adequate ventricu-
lar rate and rarely is symptomatic. It usually is transient and
does not require temporary pacing. 27 In the Mobitz type II
AV block, an intermittent block of atrial impulses occurs,
with a constant PR interval (see Fig. 27-13). It frequently ac-
companies anterior wall myocardial infarction and can re-
quire temporary or permanent pacing. This condition is
associated with a high mortality rate. In addition, Mobitz
type II AV block is associated with other types of organic
heart disease and often progresses to complete heart block.
Third-Degree AV Block. Third-degree, or complete, AV
block occurs when the conduction link for all impulses
from the SA node and atria through the AV node is
blocked, resulting in depolarization of the atria and ven-
tricles being controlled by separate pacemakers (see Fig.
27-13). The atrial pacemaker can be sinus or ectopic in ori-
gin. The ventricular pacemaker usually is located just
below the region of the block. The atria usually continue
to beat at a normal rate, and the ventricles develop their
own rate, which normally is slow (30 to 40 beats per
minute). The atrial and ventricular rates are regular but
dissociated. Third-degree AV block can result from an
interruption at the level of the AV node, in the bundle of
His, or in the Purkinje system. Third-degree blocks at the
level of the AV node usually are congenital, whereas blocks
in the Purkinje system usually are acquired. Normal QRS
complexes, with rates ranging from 40 to 60 complexes
per minute, usually are displayed on the ECG when the
block occurs proximal to the bundle of His.
Complete heart block causes a decrease in cardiac out-
put with possible periods of syncope (fainting), known as
a Stokes-Adams attack.1 Other symptoms include dizziness,
fatigue, exercise intolerance, or episodes of acute heart
failure. Most persons with complete heart block require a
permanent cardiac pacemaker.
The diagnosis of disorders of cardiac rhythm and conduc-
tion usually is made on the basis of the surface ECG. Further
clarification of conduction defects and cardiac arrhythmias
can be obtained using electrophysiologic studies.
A resting surface ECG records the impulses originating
in the heart as they are recorded at the body surface. These
impulses are recorded for a limited time and during peri-
ods of inactivity. Although there are no complications re-
lated to the procedure, errors related to misdiagnosis may
result in iatrogenic heart disease.3 The resting ECG is the
first approach to the clinical diagnosis of disorders of car-
diac rhythm and conduction but it is limited to events
that occur during the period the ECG is being monitored.
Signal-Averaged Electrocardiogram
Signal-averaged ECG is a special type of ECG that is used to
detect ventricular late action potentials that are thought to
596 UNIT VI Cardiovascular Function
originate from slow-conducting areas of the myocardium.
Ventricular late action potentials are low-amplitude, high-
frequency waveforms in the terminal QRS complex, and
they persist for tens of milliseconds into the ST segment.51
The presence of late potentials indicates high risk for de-
velopment of ventricular tachycardia and sudden cardiac
death. These late potentials are detectable from leads of
the surface ECG when signal averaging is performed.
The intent of signal averaging is reduction of noise
that makes surface ECG analysis more difficult to inter-
pret. This technique averages together multiple samples of
QRS waveforms and creates a tracing that is an average of
all the repetitive signals. Signal averaging can be carried
out by using either temporal or spatial averaging. Both ap-
proaches are based on the assumption that the noise is
random and that the signal of interest is coherent and
repetitive. 52 As a result, when several inputs that represent
the same event are combined, the coherent signal will be
reinforced, and the noise will cancel itself.
Temporal averaging is frequently referred to as signal
averaging. Most studies use temporal averaging as opposed
to spatial averaging because it affords greater noise reduc-
tion. Six standard bipolar orthogonal leads and one ground
are typically used over a large number of beats (generally
100 or more). Theoretically, this method allows for noise
reduction by a factor of 10 or more.52 The implicit assump-
tion underlying signal averaging is that the waveform is
repetitive and can be captured without loss of beat-to-beat
synchronization.
Spatial averaging uses from 4 to 16 electrodes,53 and
the inputs are averaged to provide noise reduction. The de-
gree of noise reduction is limited by the number of elec-
trodes that can be placed, the potential that closely spaced
electrodes will respond to a common noise source and not
cancel effectively, and the theoretical limit of a two-fold to
four-fold reduction in noise.52 The advantage of using spa-
tial averaging is that it enhances one’s ability to provide a
signal-averaged ECG from a single beat, thereby permit-
ting beat-to-beat analysis of transient events and complex
arrhythmias.
Signal averaging is a computer-based process. Each
electrode input is amplified, its voltage is sampled or mea-
sured at intervals of 1 msec or less, and each sample is con-
verted into a digital number with at least 12-bit precision.54
The ECG waveform is converted from an analog waveform
to digital numbers that become a computer-readable ECG.
Holter Monitoring
Holter monitoring is one form of long-term monitoring
during which a person wears a device that digitally records
two or three ECG leads for up to 48 hours. During this
time, the person keeps a diary of his or her activities or
symptoms, which later are correlated with the ECG record-
ing. Most recording devices also have an event marker but-
ton that can be pressed when the individual experiences
symptoms, which assists the technician or physician in
correlating the diary, symptoms, and ECG changes dur-
ing analysis. Holter monitoring is useful for documenting
arrhythmias, conduction abnormalities, and ST-segment
changes. The interpretative accuracy of long-term Holter
recordings varies with the system used and clinician ex-
pertise. Most computer software packages used to scan
Holter recordings are sufficiently accurate to meet clinical
demand. The majority of patients who have ischemic heart
disease exhibit premature ventricular complexes, particu-
larly those who have recently experienced myocardial in-
farction.55 The frequency of premature ventricular com-
plexes increases progressively over the first several weeks,
and it decreases approximately 6 months after infarction.
Holter recordings also are used to determine antiarrhythmic
drug efficacy, episodes of myocardial ischemia, and heart
rate variability.
Intermittent ECG recorders also are used in the diag-
nosis of arrhythmias and conduction defects. There are
two basic types of recorders that perform this type of mon-
itoring.56 The first continuously monitors rhythm and is
programmed to recognize abnormalities. In the second va-
riety, the unit does not continuously monitor the ECG
and therefore cannot automatically recognize abnormali-
ties. This latter form relies on the person to activate the
unit when he or she is symptomatic. The data are stored in
memory or transmitted telephonically to an electrocardio-
graphic receiver, where they are recorded. These types of
ECG recordings are useful in persons who have transient
symptoms.
Exercise Stress Testing
The exercise stress test elicits the body’s response to mea-
sured increases in acute exercise (see Chapter 26). This
technique provides information about changes in heart
rate, blood pressure, respiration, and perceived level of ex-
ercise. It is useful in determining exercise-induced alter-
ations in hemodynamic response and ischemic-type ECG
ST-segment changes, and it can detect and classify distur-
bances in cardiac rhythm and conduction associated with
exercise. These changes are indicative of a poorer prog-
nosis in persons with known coronary disease and recent
myocardial infarction.
Electrophysiologic Studies
An electrophysiologic study involves the passage of two or
more electrode catheters into the right side of the heart.
These catheters are inserted into the femoral, subclavian,
internal jugular, or antecubital veins and positioned with
fluoroscopy into the high right atrium near the sinus
node, the area of the His bundle, the coronary sinus that
lies in the posterior AV groove, and into the right ventri-
cle.7 The electrode catheters are used to stimulate the heart
and record intracardiac ECGs. During the study, overdrive
pacing, cardioversion, or defibrillation may be necessary
to terminate tachycardia induced during the stimulation
procedures.
Electrophysiologic studies are performed for diagnos-
tic or therapeutic purposes. A diagnostic study is performed
to determine a person’s potential for arrhythmia forma-
tion. Electrophysiologic testing also defines reproducible
arrhythmia induction characteristics and, as a result, can
be used to evaluate the therapeutic efficacy of a particular
treatment modality. Diagnostic studies can locate arrhyth-
mia foci for therapeutic intervention as well.

Therapeutic electrophysiologic studies are used as in-
terventions. These interventions may include pacing a per-
son out of tachycardia or ablation therapy. Both types of
electrophysiologic testing may be done repeatedly to test
patient responses to drugs, devices such as implantable de-
fibrillators, and surgical interventions used in the treat-
ment of arrhythmias.
Risks associated with electrophysiologic studies are
small.57 Most electrophysiologic studies do not involve
left-sided heart access, and therefore the risk for myocar-
dial infarction, stroke, or systemic embolism is less than
observed with coronary arteriography. The addition of
therapeutic maneuvers, such as ablation therapy, to the
procedure increases the risk for complications.58 Predictors
of major complications include an ejection fraction of less
than 35% and multiple ablation targets.59
QT Dispersion
A hallmark of reentrant arrhythmias is heterogeneity in re-
fractoriness and conduction velocity. An index of the
heterogeneity of ventricular refractoriness is found by ex-
amining the differences in the length of QT intervals using
the surface ECG. The most common index used to exam-
ine QT dispersion is the difference between the longest
and shortest QTc interval on the 12-lead ECG. Unusually
high QT dispersion has been associated with the risk for
life-threatening arrhythmias in a variety of disorders,60 but
these results have been inconsistent.61,62 Many different
techniques exist for determining QT dispersion, often mak-
ing it difficult to compare results of various studies. The
utility of QT dispersion is not established as yet.28
TREATMENT
The treatment of cardiac rhythm or conduction disorders is
directed toward controlling the arrhythmia, correcting the
cause, and preventing more serious or fatal arrhythmias.
Correction may involve simply adjusting an electrolyte dis-
turbance or withholding a medication such as digitalis. Pre-
venting more serious arrhythmias often involves drug
therapy, electrical stimulation, or surgical intervention.
Pharmacologic Treatment
Antiarrhythmic drugs act by modifying disordered forma-
tion and conduction of impulses that induce cardiac mus-
cle contraction. These drugs are classified into four major
groups according to the drug’s effect on the action poten-
tial of the cardiac cells. Although drugs in one category
have similar effects on conduction, they may vary signifi-
cantly in their hemodynamic effects.
Class I drugs act by blocking the fast sodium channels.
The drugs affect impulse conduction, excitability, and
automaticity to various degrees and therefore have been di-
vided further into three groups: IA, IB, and IC. Class IA
drugs (e.g., quinidine, procainamide, disopyramide) de-
crease automaticity by depressing phase 4 of the action po-
tential, decrease conductivity by moderately prolonging
phase 0, and prolong repolarization by extending phase 3
of the action potential. Because these drugs are effective in
suppressing ectopic foci and in treating reentrant arrhyth-
CHAPTER 27 Cardiac Conduction and Rhythm Disorders 597
mias, they are used for supraventricular and ventricular
arrhythmias. Class IB drugs (e.g., lidocaine, phenytoin, me-
xiletine) decrease automaticity by depressing phase 4 of the
action potential, have little effect on conductivity, decrease
refractoriness by decreasing phase 2, and shorten repolar-
ization by decreasing phase 3. Drugs in this group are used
for treating ventricular arrhythmias only and have little
or no effect on myocardial contractility. Class IC drugs
(e.g., flecainide, propafenone, moricizine) decrease conduc-
tivity by markedly depressing phase 0 of the action poten-
tial but have little effect on refractoriness or repolarization.
Drugs in this class are used for life-threatening ventricular
arrhythmias and supraventricular tachycardias.
Class II agents (e.g., propranolol, nadolol, atenolol,
timolol, acebutolol, metoprolol, pindolol, esmolol) are
β-adrenergic–blocking drugs that act by blunting the effect
of sympathetic nervous system stimulation on the heart.
These drugs decrease automaticity by depressing phase 4
of the action potential; they also decrease heart rate and
cardiac contractility. These medications are effective for
treatment of supraventricular arrhythmias and tachy-
arrhythmias secondary to excessive sympathetic activity,
but they are not very effective in treating severe arrhyth-
mias such as recurrent ventricular tachycardia.63
Class III drugs (e.g., amiodarone, bretylium, sotalol)
act by extending the action potential and refractoriness.
These agents are used in the treatment of serious ventric-
ular arrhythmias.28
Class IV drugs (e.g., verapamil, diltiazem, nifedipine,
bepridil, nitrendipine, felodipine, isradipine, nicardipine)
act by blocking the slow calcium channels, thereby de-
pressing phase 4 and lengthening phases 1 and 2. By block-
ing the release of intracellular calcium ions, these agents
reduce the force of myocardial contractility, thereby de-
creasing myocardial oxygen demand. These drugs are used
to slow the ventricular response in atrial tachycardias and to
terminate reentrant paroxysmal supraventricular tachycar-
dias when the AV node functions as a reentrant pathway.28
Two other types of antiarrhythmic drugs, the cardiac
glycosides and adenosine, are not included in this classifi-
cation schema. The cardiac glycosides (i.e., digitalis drugs)
slow the heart rate and are used in the management of ar-
rhythmias such as atrial tachycardia, atrial flutter, and atrial
fibrillation. Adenosine, an endogenous nucleoside that is
present in every cell, is used for emergency intravenous
treatment of paroxysmal supraventricular tachycardia in-
volving the AV node. It interrupts AV node conduction and
slows SA node firing.
Electrical Interventions
The correction of conduction defects, bradycardias, and
tachycardias can involve the use of an electronic pace-
maker, cardioversion, or defibrillation. Electrical interven-
tions can be used in emergency and elective situations.
Efforts directed at cardiac electrostimulation date back
more than a century. During this time, tremendous strides
have been made in the effectiveness of cardiac pacing. A
cardiac pacemaker is an electronic device that delivers an
electrical stimulus to the heart. It is used to initiate heart-
beats in situations in which the normal pacemaker of the
598 UNIT VI Cardiovascular Function
heart is defective, with certain types of AV heart block,
symptomatic bradycardia in which the rate of cardiac con-
traction and consequent cardiac output is inadequate to
perfuse vital tissues, as well as other cardiac arrhythmias.
A pacemaker may be used as a temporary or a permanent
measure. Pacemakers can pace the atria, the ventricles, or
the atria and ventricles sequentially, or overdrive pacing
can be used. Overdrive pacing is used to treat recurrent
ventricular tachycardia and reentrant atrial or ventricular
tachyarrhythmias, and to terminate atrial flutter.
Temporary pacemakers are useful for treatment of
symptomatic bradycardias and to perform overdrive pac-
ing. They can be placed transcutaneously, transvenously,
or epicardially. External temporary pacing, also known as
transcutaneous pacing, involves the placement of large patch
electrodes on the anterior and posterior chest wall, which
then are connected by a cable to an external pulse gener-
ator. Many defibrillators today have transcutaneous pac-
ing capabilities as well. Internal temporary pacing, also
known as transvenous pacing, involves the passage of a ve-
nous catheter with electrodes on its tip into the right
atrium or ventricle, where it is wedged against the endo-
cardium. The electrode then is attached to an external pulse
generator. This procedure is performed under fluoroscopic
or electrocardiographic direction. During open thoracot-
omy procedures, epicardial pacing wires sometimes are
placed. These wires are brought out directly through the
chest wall and also can be attached to an external pulse gen-
erator, if necessary.
Permanent cardiac pacemakers may become necessary
for a variety of reasons. Permanent pacemakers require im-
plantation of pacing wires into the epicardium and a pulse
generator. The pulse generator typically weighs approxi-
mately 25 to 40 g.64 Ongoing evaluation of the pacemaker’s
sensing and firing capabilities is necessary.
Synchronized cardioversion is used to terminate tachy-
cardias due to reentry, such as atrial fibrillation and most
forms of ventricular tachycardia, and defibrillation is used
as a life-saving intervention in ventricular fibrillation. The
discharge of electrical energy that is synchronized with the
R wave of the ECG is referred to as synchronized cardioversion,
and unsynchronized discharge is known as defibrillation.
The goal of both of these techniques is to provide an electri-
cal pulse to the heart in such a way as to depolarize the heart
completely during passage of the current. This electrical cur-
rent interrupts the disorganized impulses, allowing the SA
node to regain control of the heart. Defibrillation and syn-
chronized cardioversion can be delivered externally through
large patch electrodes on the chest or internally through
small paddle electrodes placed directly on the myocardium,
patch electrodes sewn into the epicardium, or transvenous
wires placed in the right ventricle. Electrical devices that
combine antitachycardial pacing, cardioversion, defibril-
lation, and bradycardial pacing are under investigation.
Automatic implantable cardioverter-defibrillators
(AICDs) are being used successfully to treat individuals
with life-threatening ventricular tachyarrhythmias by the
use of intrathoracic electrical countershock.65 Reliable sens-
ing and detection of ventricular tachyarrhythmias is es-
sential for proper functioning of the AICD. Sensing and
detection are accomplished by means of endocardial leads.
The AICD responds to ventricular tachyarrhythmias by de-
livering an electrical shock between intrathoracic elec-
trodes within 10 to 20 seconds of its onset. This time frame
provides nearly a 100% likelihood of reversal of the ar-
rhythmia, supporting the utility of this device as a reliable
and effective means of preventing sudden cardiac death in
survivors of out-of-hospital cardiac arrest.
Ablation and Surgical Interventions
Ablation therapy is used for treating recurrent, life-threat-
ening supraventricular and ventricular tachyarrhythmias.
It involves localized destruction, isolation, or excision of
cardiac tissue that is considered to be arrhythmogenic.7,28
Ablative therapy may be performed by catheter or surgical
techniques. Radiofrequency ablation uses radiofrequency
energy waves to destroy defective or aberrant electrical
conduction pathways. Cryoablation is the direct applica-
tion of an extremely cold probe to arrhythmogenic cardiac
tissue that causes freezing and necrosis of defective or aber-
rant electrical conduction pathways. The major complica-
tion with surgical ablation techniques is the perioperative
mortality rate of 5% to 15%.7 There also has been a high
morbidity rate reported.
Additional surgical interventions such as coronary
artery bypass surgery, ventriculotomy, and endocardial re-
section may be used to improve myocardial oxygenation,
remove arrhythmogenic foci, or alter electrical conduction
pathways. Coronary artery bypass surgery improves myo-
cardial oxygenation by increasing blood supply to the
myocardium. Ventriculotomy involves the removal of
aneurysm tissue and the resuturing of the myocardial walls
to eliminate the paradoxical ventricular movement and the
foci of arrhythmias. In endocardial resection, endocardial
tissue that has been identified as arrhythmogenic through
the use of electrophysiologic testing or intraoperative map-
ping is surgically removed. Ventriculotomy and endocar-
dial resection have been performed with cryoablation or
laser ablation as an adjunctive therapy.28 Other surgical
techniques, including transvenous electrocoagulation66 and
laser ablation,67 are under investigation as potential treat-
ment modalities for recurrent tachycardias.
In summary, disorders of cardiac rhythm arise as the result
of disturbances in impulse generation or conduction in the
heart. Normal sinus rhythm and respiratory sinus arrhythmia
(i.e., heart rate speeds up and slows down in concert with res-
piratory cycle) are considered normal cardiac rhythms. Cardiac
arrhythmias are not necessarily pathologic; they occur in
healthy and diseased hearts. Sinus arrhythmias originate in the
SA node. They include sinus bradycardia (heart rate <60 beats
per minute); sinus tachycardia (heart rate >100 beats per
minute); sinus arrest, in which there are prolonged periods of
asystole; and sick sinus syndrome, a condition characterized by
periods of bradycardia alternating with tachycardia.
Atrial arrhythmias arise from alterations in impulse gener-
ation that occur in the conduction pathways or muscle of the
atria. They include atrial premature contractions, atrial flutter
(i.e., atrial depolarization rate of 240 to 450 beats per minute),

and atrial fibrillation (i.e., grossly disorganized atrial depolar-
ization that is irregular with regard to rate and rhythm). Atrial
arrhythmias often go unnoticed unless they are transmitted to
the ventricles.
Arrhythmias that arise in the ventricles commonly are con-
sidered more serious than those that arise in the atria because
they afford the potential for interfering with the pumping ac-
tion of the heart. The long QT syndrome represents a prolon-
gation of the QT interval that may result in torsades de pointes
and sudden cardiac death. PVCs are caused by a ventricular
ectopic pacemaker. Ventricular tachycardia is characterized by
a ventricular rate of 70 to 250 beats per minute. Ventricular fib-
rillation (e.g., ventricular rate >350 beats per minute) is a fatal
arrhythmia unless it is successfully treated with defibrillation.
Alterations in the conduction of impulses through the AV
node lead to disturbances in the transmission of impulses from
the atria to the ventricles. There can be a delay in transmission
(i.e., first-degree heart block), failure to conduct one or more
impulses (i.e., second-degree heart block), or complete failure
to conduct impulses between the atria and the ventricles
(i.e., third-degree heart block). Conduction disorders of the
bundle of His and Purkinje system, called bundle branch blocks,
cause a widening of and changes in the configuration of the
QRS complex of the ECG.
The diagnosis of disorders of cardiac rhythm and conduc-
tion typically is accomplished using surface ECG recordings or
electrophysiologic studies. Surface electrodes can be used to
obtain a 12-lead ECG; signal-averaged electrocardiographic
studies in which multiple samples of QRS waves are averaged
to detect ventricular late action potentials; and Holter moni-
toring, which provides continuous ECG recordings for up to
48 hours. Electrophysiologic studies use electrode catheters in-
serted into the right heart by way of a peripheral vein as a
means of directly stimulating the heart while obtaining an
intracardiac ECG recording.
Both electrical devices and medications are used in the
treatment of arrhythmias and conduction disorders. Tempo-
rary and permanent cardiac pacemakers are used to treat
symptomatic bradycardias or to provide overdrive pacing pro-
cedures. Defibrillation is used to treat ventricular fibrillation.
Synchronized cardioversion procedures are carried out to treat
atrial fibrillation and ventricular tachycardia. These can be ex-
ternal or internally implanted devices. They deliver an electri-
cal charge to the myocardium in order to depolarize the heart
completely, supplying the SA node with an opportunity to take
over as the primary pacemaker of the heart. Radiofrequency
ablation and cryoablation therapy are used to destroy specific
irritable foci in the heart. Surgical procedures can be performed
to excise irritable or dysfunctional tissue, replace cardiac valves,
or provide better blood supply to the myocardial muscle wall.
REVIEW EXERCISES
A 63-year-old woman with a history of congestive heart
failure comes to the clinic complaining of feeling tired.
Her heart rate is 97 beats per minute, and the rhythm is
irregularly irregular.
CHAPTER 27 Cardiac Conduction and Rhythm Disorders 599
A. What type of arrhythmia do you think she might be
having? What would it look like if you were to ob-
tain an ECG?
B. What causes this irregularity?
C. Why do you think she is feeling tired?
D. What are some of the concerns with this type of
arrhythmia?
A 42-year-old man appears at the urgent care center with
complaints of chest discomfort, shortness of breath, and
generally not feeling well. You assess vital signs and find
that he has a temperature of 99.2°F, blood pressure of
166/90 mm HG, pulse of 87 beats per minute and
slightly irregular, and respiratory rate of 26 breaths per
minute. You perform an ECG and find that he is experi-
encing an ischemic episode in his anterior leads.
A. You attach him to a cardiac monitor and see that his
underlying rhythm is normal sinus rhythm, but he
is having frequent premature contractions that are
more than 0.10 sec in duration. You suspect that
these are what type of premature contractions?
B. What would you expect his pulse to feel like?
C. What type of ECG monitoring is indicated for this
man?
D. What do you think the etiology of this arrhythmia
might be? How might it be treated?
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