Conduction of Heart

CARDIAC CONDUCTION SYSTEMAction Potentials

Cardiac Action PotentialAbsolute and Relative Refractory Periods

Electrocardiography

DISORDERS OF CARDIAC RHYTHM AND CONDUCTION

Mechanisms of Arrhythmias and Conduction Disorders

Types of ArrhythmiasSinus Node ArrhythmiasArrhythmias of Atrial OriginJunctional ArrhythmiasDisorders of Ventricular Conduction and RhythmLong QT Syndrome and Torsades de PointesVentricular ArrhythmiasDisorders of Atrioventricular Conduction

Diagnostic MethodsSignal-Averaged ElectrocardiogramHolter MonitoringExercise Stress TestingElectrophysiologic StudiesQT Dispersion

TreatmentPharmacologic TreatmentElectrical InterventionsAblational and Surgical Interventions

Heart muscle is unique among other muscles in thatit is capable of generating and rapidly conductingits own electrical impulses or action potentials.

These action potentials result in excitation of muscle fi-bers throughout the myocardium. Impulse formation andconduction result in weak electrical currents that spreadthrough the entire body. These impulses are recorded onan electrocardiogram. Disorders of cardiac impulse gener-ation and conduction range from benign arrhythmias thatare merely annoying to those causing serious disruption ofheart function and sudden cardiac death.

581

C H A P T E R

27Cardiac Conduction andRhythm DisordersJill M. White Winters

Cardiac Conduction System

After completing this section of the chapter, you should be able tomeet the following objectives:

✦ Describe the cardiac conduction system and relate it tothe mechanical functioning of the heart

✦ Characterize the four phases of a cardiac action potentialand differentiate between the fast and slow responses

✦ Draw an ECG tracing and state the origin of thecomponent parts of the tracing

✦ Provide rationale for the importance of careful leadplacement and monitoring of ischemic events

In certain areas of the heart, the myocardial cells havebeen modified to form the specialized cells of the conduc-tion system. Although most myocardial cells are capableof initiating and conducting impulses, it is the conductionsystem that maintains the pumping efficiency of the heart.Specialized pacemaker cells generate impulses at a fasterrate than other types of heart tissue, and the conductiontissue transmits these impulses at a more rapid rate thanother cardiac cell types. Because of these properties, the con-duction system usually controls the rhythm of the heart.Blood reaches the conduction tissues by way of the coro-nary blood vessels. Coronary heart disease that interruptsblood flow through the vessels supplying tissues of theconduction system can induce serious and sometimes fataldisturbances in cardiac rhythm.

The specialized excitatory and conduction system ofthe heart consists of the sinoatrial (SA) node, in which thenormal rhythmic impulse is generated; the internodalpathways between the atria and the ventricles; the atrio-ventricular (AV) node and bundle of His, which conduct theimpulse from the atria to the ventricles; and the Purkinjefibers, 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 thepacemaker of the heart. It is a spindle-shaped strip of spe-cialized muscle tissue, about 10 to 20 mm in length and 2to 3 mm wide, located in the posterior wall of the right

atrium just below of the opening of the superior vena cavaand less than 1 mm from the epicardial surface.1 Bloodsupply to the SA node is provided by means of the cir-cumflex artery. It has been suggested that no single cell inthe SA node serves as the pacemaker, but rather that sinusnodal cells discharge synchronously because of mutualentrainment.2 As a result, the firing of faster-dischargingcells is slowed down by slower-discharging cells, and thefiring rate of slower-discharging cells is sped up by faster-discharging cells, resulting in a synchronization of theirfiring rate.

Impulses originating in the SA node travel throughthe atria to the AV node. Because of the anatomic locationof 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 beforethe 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 anastomoseproximal to the AV node. Interatrial conduction appears tobe accomplished through Bachmann’s bundle. This largemuscle bundle originates along the anterior border of theSA node and travels posteriorly around the aorta to the leftatrium.4

The heart essentially has two conduction systems: onethat 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 atriaand ventricles. The AV node is a compact ovoid structuremeasuring approximately 1 × 3 × 5 mm, which is locatedslightly beneath the right atrial endocardium, anterior tothe opening of the coronary sinus, and immediately abovethe insertion of the septal leaflet of the tricuspid valve.1,4 In85% to 90% of people, blood supply to the AV node is pro-vided by the right coronary artery.1 The AV node is dividedinto three functional regions: the AN, or transitional, zonebetween the atria and the rest of the node; the middle N,or nodal, zone; and the NH, or upper, zone of the ventric-

ular conduction system.5 Within the AN portion of thenode, atrial fibers connect with very small junctional fibersof the node itself. The velocity of conduction through theAN and N fibers is very slow (approximately one half thatof normal cardiac muscle), which greatly delays transmis-sion of the impulse.5,6 A further delay occurs as the impulsetravels through the nodal region into the NH region, whichconnects with the bundle of His (also called the AV bundle).This delay provides a mechanical advantage whereby theatria complete their ejection of blood before ventricularcontraction begins. Under normal circumstances, the AVnode provides the only connection between the atrial and

582 UNIT VI Cardiovascular Function

SA node AVnode

Bundle ofHis Left

posteriorfascicle

Leftanteriorfascicle

Purkinjefibers

Right bundlebranch Left bundle

branch

A

B

C

FIGURE 27-1 Conduction system of the heart andaction 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.

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, whichhas 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, ordiastolic repolarization period.

➤ Cardiac muscle has two types of ion channels that functionin producing the voltage changes that occur during the de-polarization phase of the action potential: the fast sodiumchannels and the slow calcium channels.

➤ There are two types of cardiac action potentials: the fast re-sponse, which occurs in atrial and ventricular muscle cellsand the Purkinje conduction system and uses the fastsodium channels; and the slow response of the SA and AV nodes, which uses the slow calcium channels.

ventricular conduction systems. The atria and ventricleswould beat independently of each other if the transmissionof impulses through the AV node were blocked.

The Purkinje system, which supplies the ventricles, haslarge fibers that allow for rapid conduction and almostsimultaneous 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 andefficient ejection of blood from the heart. The fibers of thePurkinje system originate in the AV node and proceed toform the bundle of His, which extends through the fibroustissue between the valves of the heart and into the ven-tricular system. Because of its proximity to the aortic valveand the mitral valve ring, the bundle of His is predisposedto inflammation and deposits of calcified debris that caninterfere with impulse conduction.6 The bundle of Hispenetrates into the ventricles and almost immediately di-vides into right and left bundle branches that straddle theinterventricular septum. Branches from the anterior andposterior descending coronary arteries provide blood sup-ply for the His bundle, making this conduction site lesssusceptible to ischemic damage, unless the damage is ex-tensive.1 The bundle branches move through the sub-endocardial tissues toward the papillary muscles and thensubdivide into the Purkinje fibers, which branch out andsupply the outer walls of the ventricles. The main trunk ofthe left bundle branch extends for approximately 1 to 2 cmbefore fanning out as it enters the septal area and dividesfurther into two segments: the left posterior and anterior fas-cicles. The left bundle branch is supplied with blood fromboth the left anterior descending artery and the posteriordescending artery (formed from the right coronary artery),whereas the right bundle branch receives its blood fromboth the right and left anterior descending coronary arte-rial systems.1

The AV nodal fibers, when not stimulated, dischargeat an intrinsic discharge rate of 40 to 60 times a minute,and the Purkinje fibers discharge at 15 to 40 times perminute. Although the AV node and Purkinje system havethe ability to control the rhythm of the heart, they do notnormally do so because the discharge rate of the SA nodeis considerably faster. Each time the SA node discharges,its impulses are conducted into the AV node and Purkinjefibers, causing them to fire. The AV node can assume thepacemaker function of the heart should the SA node fail todischarge, and the Purkinje system can assume the pace-maker function of the ventricles should the AV node failto conduct impulses from the atria to the ventricles. Shouldthis occur, the heart rate will reflect the intrinsic firing rateof 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 takeplace in the heart are responsible for initiating each cardiaccontraction. An action potential can be divided into threephases: the resting or unexcited state, depolarization, andrepolarization.

The inside of a cardiac cell, like all living cells, containsa negative electrical charge compared with the outside ofthe cell. During the resting state, the membrane is relativelypermeable to potassium but much less so to sodium andcalcium.6 Charges of opposite polarity become alignedalong the membrane (positive on the outside and negativeon the inside; Fig. 27-2).

Depolarization occurs when the cell membrane sud-denly becomes selectively permeable to current-carryingions such as sodium. Sodium ions enter the cell and resultin a sharp rise of the intracellular potential to positivity.

Repolarization involves reestablishment of the restingmembrane potential. It is a complex and somewhat slowerprocess, involving the outward flow of electrical chargesand the return of membrane potential to its resting state.7

During repolarization, the membrane conductance or per-meability for potassium greatly increases, allowing thepositively charged potassium ions to move outward acrossthe membrane. This outward movement of potassiumremoves positive charges from inside the cell; thus, themembrane again becomes negative on the inside and pos-itive on the outside. The sodium-potassium membranepump also assists in repolarization by pumping positivelycharged sodium ions out across the cell membrane.8

Cardiac Action PotentialThe action potential in cardiac muscle is typically dividedinto 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 threetypes of membrane ion channels that contribute to thevoltage changes that occur during the phases of the cardiacaction potential. They are the fast sodium channels, the slowcalcium channels, and the potassium channels.

During phase 0, in atrial and ventricular muscle and inthe Purkinje system, the fast sodium channels in the cellmembrane are stimulated to open, resulting in the rapid in-flux of sodium. The action potentials in the normal SA andAV nodes have a much slower upstroke and are mediatedpredominantly by the slow calcium currents. The point atwhich the sodium gates open is called the depolarization

CHAPTER 27 Cardiac Conduction and Rhythm Disorders 583

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 ofcharge across the membrane, and repolarization denotes the returnof the membrane potential to its resting state.

threshold. When the cell has reached this threshold, a rapidinflux of sodium occurs. The exterior of the cell now isnegatively charged in relation to the highly positive inte-rior of the cell. This rapid influx of sodium produces arapid, positively directed change in the transmembranepotential, resulting in the electrical spike and overshootduring phase 0 of the action potential.7 The membranepotential shifts from a resting membrane potential of ap-proximately −90 millivolts (mV) to +20 mV (Fig. 27-4). Therapid 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 tocause adjacent cells to depolarize because the voltage spikeof the cell’s depolarization stimulates the sodium channelsin nearby cells to open. Therefore, when a cardiac cell isstimulated 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 andsignifies inactivation of the fast sodium channels with anabrupt decrease in sodium permeability. The slight down-ward slope is thought to be caused by the influx of a smallamount of negatively charged chloride ions and efflux ofpotassium.1 The decrease in intracellular positivity reducesthe membrane potential to a level near 0 mV, from whichthe plateau, or phase 2, arises.

Phase 2 represents the plateau of the action potential.If potassium permeability increased to its resting level atthis time, as it does in nerve fibers or skeletal muscle, thecell would repolarize rapidly. Instead, potassium perme-ability is low, allowing the membrane to remain depolar-ized throughout the phase 2 plateau. A concomitant influxof calcium into the cell through slow channels contributesto the phase 2 plateau.7 Calcium ions entering the muscleduring this phase also play a key role in the contractileprocess.1 These unique features of the phase 2 plateau inthese cells cause the action potential of cardiac muscle(several hundred milliseconds) to last 3 to 15 times longerthan 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 beginswith the downslope of the action potential. During thephase 3 repolarization period, the slow channels close,and the influx of calcium and sodium ceases. There is asharp rise in potassium permeability, contributing to therapid outward movement of potassium and reestablish-ment of the resting membrane potential (−90 mV). At theconclusion of phase 3, the distribution of potassium andsodium returns membrane to the normal resting state.The T wave on the ECG corresponds with phase 3 of theaction potential.

Phase 4 represents the resting membrane potential.During phase 4, the activity of the sodium-potassium pumpcontributes to maintenance of the resting membrane po-tential by transporting sodium out of the cell and movingpotassium back in. Phase 4 corresponds to diastole.

The Fast and Slow Response. There are two main types ofaction potentials in the heart—the fast response and theslow response (see Fig. 27-4). The fast response occurs in thenormal myocardial cells of the atria, the ventricles, and thePurkinje 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 thespecialized cells of the SA node are conducted to the fast-response myocardial cells, where they effect a change inmembrane potential to the threshold level. On reachingthreshold, the voltage-dependent sodium channels open toinitiate the rapid upstroke of the phase 1 action potential.The amplitude and the rate of rise of phase 1 are importantto the conduction velocity of the fast response. Myocardialfibers 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 thenatural pacemaker of the heart, and in the conductionfibers of the AV node (see Fig. 27-4). The hallmark of thesepacemaker cells is a spontaneous phase 4 depolarization.The membrane permeability of these cells allows a slowinward leak of current to occur through the slow channelsduring phase 4. This leak continues until the threshold forfiring is reached, at which point the cell spontaneously de-polarizes. Under normal conditions, the slow response,


Thresholdpotential

Baseline

P

Delay inAV node

Depolarizationof atria

Depolarizationof ventricles

Repolarizationof ventricles

R

Q

S

T

U

0

1

2

3

4Resting

membranepotential

FIGURE 27-3 Relation between (A) the electrocardiogram and (B) phases of the ventricular action potential.

A

B

sometimes referred to as the calcium current, does not con-tribute significantly to myocardial depolarization in theatria and ventricles. Its primary role in normal atrial andventricular cells is to provide for the entrance of calciumfor the excitation-contraction mechanism that couples theelectrical activity with muscle contraction.

The rate of pacemaker cell discharge varies with theresting 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 byincreasing the slope or rate of phase 4 depolarization.Acetylcholine, which is released during vagal stimulationof the heart, slows the heart rate by decreasing the slopeof phase 4.

The fast response of atrial and ventricular muscle canbe converted to a slow pacemaker response under certain

conditions. For example, such conversions may occur spon-taneously in individuals with severe coronary artery disease,in areas of the heart where blood supply has been markedlycompromised or curtailed. Impulses generated by these cellscan lead to ectopic beats and serious arrhythmias.

Absolute and Relative Refractory PeriodsThe pumping action of the heart requires alternating con-traction and relaxation. There is a period in the action po-tential curve during which no stimuli can generate anotheraction potential (Fig. 27-5). This period, which is known asthe absolute refractory period, includes phases 0, 1, 2, and partof phase 3. During this time, the cell cannot depolarizeagain under any circumstances. When repolarization hasreturned the membrane potential to below threshold, al-though not to the resting membrane potential (−90 mV),the cell is capable of responding to a greater-than-normalstimulus. This condition is referred to as the relative refrac-tory period. The relative refractory period begins when thetransmembrane potential in phase 3 reaches the thresholdpotential level and ends just before the terminal portion ofphase 3. After the relative refractory period is a short period,called the supernormal excitatory period, during which a weakstimulus can evoke a response. The supernormal excitatoryperiod extends from the terminal portion of phase 3 untilthe beginning of phase 4. It is during this period that cardiacarrhythmias develop.

In skeletal muscle, the refractory period is very shortcompared with the duration of contraction, such that asecond contraction can be initiated before the first is over,resulting in a summated tetanized contraction. In cardiacmuscle, the absolute refractory period is almost as long as the contraction, and a second contraction cannot bestimulated until the first is over. The longer length of the


A

B

2

3

4

0

Mill

ivol

ts

Time (msec)

+20

0

-20

-40

-60

-80

-90

+20

0

-20

-40

-60

-80

-90

Threshold

4

0

1

2

3

FIGURE 27-4 Changes in action potential recorded from a fast re-sponse in cardiac muscle cell (top) and from a slow responserecorded in the sinoatrial and atrioventricular nodes (bottom). Thephases of the action potential are identified by numbers: phase 4,resting membrane potential; phase 0, depolarization; phase 1, briefperiod of repolarization; phase 2, plateau; phase 3, repolarization.The slow response is characterized by a slow, spontaneous rise inthe phase 4 membrane potential to threshold levels; it has a lesseramplitude and shorter duration than the fast response. Increasedautomaticity (A) occurs when the rate of phase 4 depolarization isincreased.

12

3

4

0

TP

RMP

ARP RRP SN

FIGURE 27-5 Diagram of an action potential of a ventricular musclecell, showing the threshold potential (TP), resting membranepotential (RMP), absolute refractory period (ARP), relative refractoryperiod (RRP), and supernormal (SN) period.

absolute refractory period of cardiac muscle is importantin maintaining the alternating contraction and relaxationthat is essential to the pumping action of the heart and forthe prevention of fatal arrhythmias.

ELECTROCARDIOGRAPHY

The electrocardiogram (ECG) is a graphic recording of theelectrical 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-trodes, amplified, and viewed on an oscilloscope or chartrecorder.

The deflection points of an ECG are designated by theletters P, Q, R, S, and T. Figure 27-6 depicts the electricalactivity of the conduction system on an ECG tracing. TheP wave represents the SA node and atrial depolarization;the QRS complex (i.e., beginning of the Q wave to the endof the S wave) depicts ventricular depolarization; and theT wave portrays ventricular repolarization. The isoelectricline between the P wave and the Q wave represents depo-larization of the AV node, bundle branches, and Purkinjesystem (Fig. 27-7). Atrial repolarization occurs during ven-tricular depolarization and is hidden in the QRS complex.

The ECG records the potential difference in charge (inmillivolts) between two electrodes as depolarization and re-polarization waves move through the heart and are con-ducted to the skin surface. The shape of the recordertracing is determined by the direction in which the im-pulse spreads through the heart muscle in relation to elec-trode placement. A depolarization wave that moves toward

the recording electrode registers as a positive, or upward,deflection. Conversely, if the impulse moves away from therecording 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 thebaseline of the chart.

The ECG recorder is much like a camera in that it canrecord different views of the electrical activity of the heart,


Delay inAV node

P

R

-0.5

0

mV

0.2Second

0.4 0.6

0

0.5

1.0

T

Q

S

UBaseline

Depolarizationof atria

Depolarizationof ventricles

Repolarizationof ventricles

P

R

T

QIsoelectric

lineS

U

QT IntervalQRS Duration

PR Interval

PR Segment ST Segment

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 duringventricular depolarization and is hidden under the QRS complex.

ECG

SA

nod

e

P wave

QRS complex

Atria

AV node

His

bun

dle

Bun

dle

bran

ches

Pur

kinj

e ne

twor

k

FIGURE 27-7 Tissues depolarized by a wave of activation com-mencing in the sinoatrial (SA) node are shown in a series of blockssuperimposed on the deflections of the electrocardiogram (ECG).(Katz A.M. [1992]. Physiology of the heart [p. 483]. New York: RavenPress)

depending on where the recording electrode is placed. Thehorizontal axis of the ECG measures time (seconds), andthe vertical axis measures the amplitude of the impulse(millivolts). Each heavy vertical line represents 0.2 second,and each thin line represents 0.04 second (see Fig. 27-6).The widths of ECG complexes are commonly referred to interms of duration of time. On the vertical axis, each heavyhorizontal line represents 0.5 mV. The connections of theECG are arranged such that an upright deflection indicatesa positive potential and a downward deflection indicates anegative potential. Although the vertical axis determinesamplitude in terms of voltage, these values frequently arecommunicated as millimeters of positive or negative de-flection rather than in millivolts.

Conventionally, 12 leads (6 limb leads and 6 chestleads) are recorded for a diagnostic ECG, each providing aunique view of the electrical forces of the heart from a dif-ferent position on the body’s surface. The six limb leadsview the electrical forces as they pass through the heart onthe frontal or vertical plane. The electrodes are attached tothe four extremities or representative areas on the bodynear the shoulders and lower chest or abdomen. The elec-trical potential recorded from any one extremity should bethe same no matter where the electrode is placed on theextremity. The six chest leads provide a view of the electri-cal forces as they pass through the heart on the horizontalplane. They are moved to different positions on the chest,including the right and left sternal borders and the left an-terior surface. The right lower extremity lead is used as aground electrode. When indicated, additional electrodesmay be applied to other areas of the body, such as the backor right anterior chest.

The goals of continuous bedside cardiac monitoringhave shifted from simple heart rate and arrhythmia mon-itoring to identification of ST-segment changes, advancedarrhythmia identification, diagnosis, and treatment. Manydiagnostic criteria are lead specific. The monitoring leadsselected must maximize the potential for accurately iden-tifying anticipated arrhythmias and ischemic events onthe basis of the patient’s underlying clinical situation.

When monitoring patients with wide QRS-complextachycardia (discussed later), the use of 12-lead ECG mon-itoring systems is considered optimal. For example, Drewand Scheinman10 found that the use of 12-lead ECG mon-itoring systems resulted in more than 90% accuracy whendiagnosing wide QRS arrhythmias; whereas the use of leadII, a limb lead commonly used for continuous monitoring,resulted in only 34% being correctly identified.

Although accurate ECG placement and lead selectionare an important aspect of ECG monitoring, two nationalsurveys conducted in 1991 and 1995, respectively,11,12 iden-tified two common errors: inaccurate electrode placementand inappropriate lead selection for individual clinical sit-uations. Improper lead placement can significantly changeQRS morphology, resulting in misdiagnosis of cardiac ar-rhythmias.13 Inappropriate lead selection can also result inconduction defects being missed.

In persons with acute coronary syndrome (ACS), in-cluding unstable angina and ST-segment elevation andnon–ST-segment elevation myocardial infarction, careful

cardiac ECG monitoring is imperative14 (see Chapter 26).Persons with ACS are at risk for developing extension ofan infarcted area, ongoing myocardial ischemia, and life-threatening arrhythmias. Research has revealed that 80%to 90% of ECG-detected ischemic events are clinicallysilent.15,16 Thus, ECG monitoring is more sensitive than apatient’s report of symptoms for identifying transientongoing myocardial ischemia. ECG monitoring also pro-vides for more accurate and timely detection of ischemicevents, essential for treatment options such as reperfusionstrategies.17 It is recommended that all 12 ECG leads beused for monitoring patients with ACS because ischemicchanges that occur may be evident in different leads at dif-ferent times.

In summary, the rhythmic contraction and relaxation of theheart rely on the specialized cells of the heart’s conduction sys-tem. Specialized cells in the SA node have the fastest inherentrate of impulse generation and act as the pacemaker of theheart. Impulses from the SA node travel through the atria tothe AV node and then to the AV bundle and the ventricularPurkinje system. The AV node provides the only connectionbetween the atrial and ventricular conduction systems. Theatria and the ventricles function independently of each otherwhen AV node conduction is blocked.

The action potential of cardiac muscle is divided into fivephases: phase 0 represents depolarization and is characterizedby the rapid upstroke of the action potential; phase 1 is char-acterized by a brief period of repolarization; phase 2 consistsof a plateau, which prolongs the duration of the action poten-tial; phase 3 represents repolarization; and phase 4 is the rest-ing membrane potential. After an action potential, there is arefractory period during which the membrane is resistant to asecond stimulus. During the absolute refractory period, themembrane is insensitive to stimulation. This period is followedby the relative refractory period, during which a more intensestimulus is needed to initiate an action potential. The relativerefractory period is followed by a supernormal excitatoryperiod, during which a weak stimulus can evoke a response.

The ECG provides a means for monitoring the electrical ac-tivity of the heart. Conventionally, 12 leads (6 limb leads and6 chest leads) are recorded for a diagnostic ECG, each provid-ing a unique view of the electrical forces of the heart from adifferent position on the body’s surface. This allows for ad-vanced arrhythmia interpretation, detection of wide QRS-complex tachycardia, and early identification of ischemic andinfarction changes in persons with ACS.

Disorders of Cardiac Rhythmand Conduction

After completing this section of the chapter, you should be able tomeet the following objectives:

✦ Describe the possible mechanisms for arrhythmiageneration

✦ Compare sinus arrhythmias with atrial arrhythmias


✦ Characterize the effects of atrial flutter and atrialfibrillation 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 oncardiac function

✦ Cite the types of cardiac conditions that can bediagnosed using the ECG

✦ Describe the methods used in diagnosis of cardiacarrhythmias

✦ Explain the mechanisms, criteria for use, and benefits ofantiarrhythmic drugs, internal cardioverter-defibrillatortherapy, ablation therapy, and surgical procedures in thetreatment of persons with recurrent, symptomaticarrhythmias

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 arrhythmiahave sometimes been used interchangeably to describe dis-orders of cardiac rhythm. Marriott18 has pointed out thatthe term arrhythmia was originally based on the usage ofthe alpha privative (the prefix a-) to imply “imperfectionin” as opposed to “absence of” cardiac rhythms. However,Marriott further pointed out that the term dysrhythmiahas not been generally accepted, and conventional use ofthe 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, myocardialischemia 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 theirharmful effects by interfering with the heart’s pumpingability. 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 manifestfour inherent properties that contribute to the genesis ofall cardiac rhythms, both normal and abnormal. They areautomaticity, excitability, conductivity, and refractoriness.An alteration in any of these four properties may producearrhythmias or conduction defects.

The ability of certain cells in the conduction systemto initiate an impulse or action potential spontaneously isreferred to as automaticity. The SA node has an inherentdischarge rate of 60 to 100 times per minute. It normallyacts as the pacemaker of the heart because it reaches the

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 isblocked, another site that is capable of automaticity takesover 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 thebundle branch Purkinje fibers. These pacemakers have aslower rate of discharge than the SA node. The AV nodehas an inherent firing rate of 40 to 60 times per minute,and the Purkinje system fires at a rate of 20 to 40 times perminute. The SA node may be functioning properly, but be-cause of additional precipitating factors, other cardiac cellscan assume accelerated properties of automaticity andbegin to initiate impulses. These additional factors mightinclude 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 thenormally functioning SA node. These pacemakers can re-side in other parts of the conduction system or in musclecells 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 conductionpathways, they are not coupled with normal mechanicalevents, and they often render the heart refractory or inca-pable of responding to the next normal impulse arising inthe SA node. They occur without incident in persons withhealthy hearts in response to sympathetic nervous systemstimulation 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 toan impulse and generate an action potential. Myocardialcells that have been injured or replaced by scar tissue do


PHYSIOLOGIC BASIS OF ARRHYTHMIAGENERATION

➤ Cardiac arrhythmias represent disorders of cardiac rhythmrelated to alterations in automaticity, excitability, conduc-tivity, or refractoriness of specialized cells in the conductionsystem of the heart.

➤ Automaticity refers to the ability of pacemaker cells in theheart to spontaneously generate an action potential. Normally, the SA node is the pacemaker of the heartbecause of its intrinsic automaticity.

➤ Excitability is the ability of cardiac tissue to respond to animpulse and generate an action potential.

➤ Conductivity and refractoriness represent the ability ofcardiac tissue to conduct action potentials.

➤ Whereas conductivity relates to the ability of cardiac tissueto conduct impulses, refractoriness represents temporaryinterruptions in conductivity related to the repolarizationphase of the action potential.

not possess normal excitability. For example, during theacute phase of an ischemic event, involved cells becomedepolarized. These ischemic cells remain electrically cou-pled to the adjacent nonischemic area; current from theischemic 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 torespond to an incoming stimulus. The refractory period ofcardiac muscle is the interval in the repolarization periodduring 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 heartin an orderly, sequential manner. The electrical impulsethen dies out and does not reenter adjacent tissue becausethat tissue has already been depolarized and is refractoryto immediate stimulation. However, fibers that were notactivated during the initial wave of depolarization can re-cover excitability before the initial impulse dies out, andthey may serve as a link to reexcite areas of the heart thatwere just discharged and have recovered from the initialdepolarization.1,19 This activity disrupts the normal con-duction sequence. For reentry to occur, there must be areasof slow conduction and unidirectional conduction block(Fig. 27-8). For previously depolarized areas to repolarizeadequately to conduct an impulse again, slow conductionis necessary. Unidirectional block is necessary to provide aone-way route for the original impulse to reenter, thereby

blocking other impulses entering from the opposite direc-tion from extinguishing the reentrant circuit. Reentry re-quires a triggering stimulus such as an extrasystole. Ifsufficient time has elapsed for the refractory period in thereentered 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 largeand include an entire specialized conduction system, or thecircuit can be microscopic. It can include myocardial tissue,AV nodal cells, junctional tissue, or the ventricles. Factorscontributing to the development of a reentrant circuit in-clude ischemia, infarction, and elevated serum potassiumlevels.22 Scar tissue interrupts the normally low-resistancepaths 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 todetect the resultant late potentials. Effects of drugs suchas epinephrine can produce a shortened refractory period,thereby increasing the likelihood of reentrant arrhythmias.

There are several forms of reentry. The first is anatomicreentry. It consists of an excitation wave that travels in aset 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, atrialfibrillation, atrial flutter, AV nodal reentry, and some ven-tricular tachycardias. Functional reentry does not rely onan anatomic structure to circle; rather, it depends on thelocal differences in conduction velocity.1,23 Spiral reentry isthe most common form of this type of reentry.24 It is initi-ated by a wave of electrical current that does not propagatenaturally in its normal plane after meeting refractory tis-sue. The broken end of the wave curls, forms a vortex, andpermanently rotates. This phenomenon suppresses normalpacemaker activity and can result in atrial fibrillation.23 Ar-rhythmias observed with functional reentry are likely to bepolymorphic because of charging circuits.1 Reflection issometimes considered another form of reentry that canoccur in parallel pathways of myocardial tissue or the Purk-inje network. With reflection, the cardiac impulse reachesthe depressed segment, triggers the surrounding tissue, andthen returns in a retrograde direction through the severelydepressed region. Reflection differs from true reentry inthat the impulse travels along the same pathway in bothdirections and does not require a circuit.1

TYPES OF ARRHYTHMIAS

Sinus Node ArrhythmiasIn a healthy heart driven by sinus node discharge, theheart rate ranges between 60 and 100 beats per minute. Onthe ECG, a P wave may be observed to precede every QRScomplex. Historically, normal sinus rhythm has been con-sidered the “normal” rhythm of a healthy heart. In normalsinus rhythm, a P wave precedes each QRS complex, andthe RR intervals, which are used to measue heart rate, re-main relatively constant over time (Fig. 27-9). Alterationsin the function of the SA node lead to changes in rate orrhythm of the heartbeat.


FIGURE 27-8 The role of unidirectional block in reentry. (A) An exci-tation wave traveling down a single bundle (S) of fibers continuesdown the left (L) and right (R) branches. The depolarization waveenters the connecting branch (C) from both ends and is extin-guished at the zone of collision. (B) The wave is blocked in the L andR branches. (C) Bidirectional block exists in branch R. (D) The ante-grade impulse is blocked, but the retrograde impulse is conductedthrough and reenters bundle S. (Berne R.M., Levy M.N. [1988]. Phys-iology [2nd ed., p. 417]. St. Louis: C.V. Mosby)

Years ago, it was believed that sinus rhythm should beregular; that is, all RR intervals should be equal. Today, itis accepted that a more optimal rhythm is respiratorysinus arrhythmia. Respiratory sinus arrhythmia is a cardiacrhythm characterized by gradual lengthening and shorten-ing of RR intervals (see Fig. 27-9). This variation in cardiaccycles is related to intrathoracic pressure changes that occurwith respiration and resultant alterations in autonomiccontrol of the SA node. Inspiration causes acceleration ofthe heart rate, and expiration causes slowing. Respiratorysinus arrhythmia accounts for most heart rate variability inhealthy individuals. Decreased heart rate variability hasbeen 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 sinusbradycardia, a P wave precedes each QRS. A normal P waveand PR interval (0.12 to 0.20 second) indicate that the im-pulse originated in the SA node rather than in another areaof the conduction system that has a slower inherent rate.Vagal stimulation decreases the firing rate of the SA nodeand conduction through the AV node to cause a decreasein heart rate. This rhythm may be normal in trained ath-letes, who maintain a large stroke volume, and duringsleep. Sinus bradycardia may be an indicator of poor prog-nosis when it occurs in conjunction with acute myocardialinfarction, particularly if associated with hypotension.

Sinus Tachycardia. Sinus tachycardia refers to a rapidheart rate (>100 beats per minute) that has its origin in theSA node (see Fig. 27-9). A normal P wave and PR intervalshould precede each QRS complex. The mechanism ofsinus tachycardia is enhanced automaticity related to sym-pathetic stimulation or withdrawal of vagal tone. Sinustachycardia is a normal response during fever and exerciseand in situations that incite sympathetic stimulation. Itmay be associated with congestive heart failure, myocardialinfarction, and hyperthyroidism. Pharmacologic agentssuch as atropine, isoproterenol, epinephrine, and quinidinealso can cause sinus tachycardia.

Sinus Arrest. Sinus arrest refers to failure of the SA node todischarge and results in an irregular pulse. An escape rhythmdevelops as another pacemaker takes over. Sinus arrestmay 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, myocardialinfarction, acute myocarditis, excessive vagal tone, quini-dine, acetylcholine, and hyperkalemia or hypokalemia.25

Sick Sinus Syndrome. Sick sinus syndrome is a term thatdescribes a number of forms of cardiac impulse formationand intra-atrial and AV conduction abnormalities.26–28 Thesyndrome most frequently is the result of total or subtotaldestruction of the SA node, areas of nodal–atrial disconti-nuity, inflammatory or degenerative changes of the nervesand ganglia surrounding the node, or pathologic changes


A

B

C

D

FIGURE 27-9 Electrocardiographic (ECG) tracings of rhythmsoriginating in the sinus node. (A) Normal sinus rhythm (60 to100 beats per minute). (B) Sinus bradycardia (<60 beats perminute). (C) Sinus tachycardia (>100 beats per minute). (D) Res-piratory sinus arrhythmia, characterized by gradually length-ening and shortening of RR intervals.

in the atrial wall.28 In addition, occlusion of the sinus nodeartery may be a significant contributing factor. Approxi-mately 40% of adults with sick sinus syndrome also havecoronary heart disease.29 In children, the syndrome is mostcommonly associated with congenital heart defects, par-ticularly following corrective cardiac surgery.28

The arrhythmias associated with sick sinus syndromeinclude spontaneous persistent sinus bradycardia that is notdrug induced or appropriate for the physiologic circum-stances, prolonged sinus pauses, combinations of SA andAV node conduction disturbances, or alternating parox-ysms of rapid regular or irregular atrial tachyarrhythmiasand periods of slow atrial and ventricular rates (bradycardia-tachycardia syndrome).30 Most commonly, the term sick si-nus syndrome is used to refer to the bradycardia-tachycardiasyndrome. The bradycardia is caused by disease of the sinusnode (or other intraatrial conduction pathways), and thetachycardia is caused by paroxysmal atrial or junctional ar-rhythmias. Individuals with this syndrome often are asymp-tomatic. Ironically, the development of atrial fibrillationmay alleviate symptoms in persons who are symptomaticbecause heart rate can be controlled more consistentlyunder these circumstances.27

The most common manifestations of sick sinus syn-drome are lightheadedness, dizziness, and syncope, symp-toms related to the bradyarrhythmias.29,31 When patientswith sick sinus syndrome experience palpitations, they aregenerally the result of tachyarrhythmias and are suggestiveof 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 drugtherapy to treat the tachycardia, is often required in brady-cardia-tachycardia syndrome.28 Medications that affect SAnode discharge must be cautiously used.

Arrhythmias of Atrial OriginImpulses from the SA node pass through the conductivepathways in the atria to the AV node. Arrhythmias of atrialorigin include premature atrial contractions, paroxysmal

supraventricular tachycardia, atrial flutter, and atrial fibril-lation (Fig. 27-10).

Premature Atrial Contractions. Premature atrial contrac-tions (PACs) are contractions that originate in the atrialconduction pathways or atrial muscle cells and occur be-fore the next expected SA node impulse. This impulse tocontract usually is transmitted to the ventricle and back tothe SA node. The location of the ectopic focus determinesthe configuration of the P wave. In general, the closer theectopic focus is to the SA node, the more the ectopic com-plex resembles a normal sinus complex. The retrogradetransmission to the SA node often interrupts the timing ofthe next sinus beat, such that a pause occurs between thetwo normally conducted beats. In healthy individuals,PACs may be the result of stress, tobacco, or caffeine. Theyalso have been associated with myocardial infarction, dig-italis toxicity, low serum potassium or magnesium levels,and hypoxia.

Paroxysmal Supraventricular Tachycardia. Paroxysmalsupraventricular tachycardia is sometimes referred to as paroxysmal atrial tachycardia. This term includes all


Atrialflutter

Onset PAT

Atrialfibrillation

Paroxysmalatrial

tachycardia(PAT)

Prematureatrial

contractions(PAC)

QRS

P P P P P P P P P P

QRS QRS

Fibrillatory P waves

P T P T P T P TP TP TP

QRS QRS QRS QRS QRSQRS

Normal sinus rhythm

PAC

QRS QRSQRS

FIGURE 27-10 Electrocardiographic tracings of atrial arrhythmias.Atrial flutter (first tracing) is characterized by the atrial flutter (F) wavesoccurring at a rate of 240 to 450 beats per minute. The ventricularrate remains regular because of the conduction of every sixth atrialcontraction. Atrial fibrillation (second tracing) has grossly disorga-nized atrial electrical activity that is irregular with respect to rate andrhythm. The ventricular response is irregular, and no distinct P wavesare visible. The third tracing illustrates paroxysmal atrial tachycardia(PAT), preceded by a normal sinus rhythm. The fourth tracing illus-trates premature atrial complexes (PAC).

SUPRAVENTRICULAR AND VENTRICULARARRHYTHMIAS

➤ Supraventricular arrhythmias represent disorders of atrialrhythm or conduction.

➤ Atrioventricular nodal and junctional arrhythmias resultfrom disruption in conduction of impulses from the atria tothe ventricles.

➤ Ventricular arrhythmias represent disorders of ventricularrhythm or conduction.

➤ Because the ventricles are pumping chambers of the heart,arrhythmias that produce an abnormally slow (e.g.,heartblock) or rapid ventricular rate (e.g., ventricular tachycardiaor fibrillation) are potentially life threatening.

tachyarrhythmias that originate above the bifurcation ofthe 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 accessoryconduction pathway between the atria and ventricles), orintraatrial or sinus node reentry. Paroxysmal supraven-tricular tachycardias tend to be recurrent and of shortduration.

Atrial Flutter. Atrial flutter is a rapid atrial ectopic tachy-cardia, with an atrial rate that ranges from 240 to 450 beatsper minute. There are two types of atrial flutter.27 Type Iflutter (classic) is the result of a reentry mechanism in theright atrium and can be entrained and interrupted withatrial pacing techniques. The atrial rate in typical type Iflutter usually is in the vicinity of 300 beats per minute,but it can range from 240 to 340 beats per minute. Themechanism 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 sawtoothpattern in leads II, III, aVF, and V1.32 The ventricular re-sponse rate and regularity are variable and depend on theAV conduction sequence. When regular, the ventricularresponse rate usually is a defined fraction of the atrial rate(i.e., when conduction from the atria to the ventricles is2�1, an atrial flutter rate of 300 would result in a ventricu-lar response rate of 150 beats per minute). The QRS complexmay be normal or abnormal, depending on the presence orabsence of preexisting intraventricular conduction defectsor aberrant ventricular conduction.

Atrial flutter rarely is seen in normal, healthy individ-uals. It may be seen in persons of any age in the presenceof underlying atrial abnormalities. Subgroups that are atparticularly high risk for development of atrial flutter in-clude children, adolescents, and young adults who haveundergone corrective surgery for complex congenital heartdiseases.27

Atrial Fibrillation. Atrial fibrillation is characterized bychaotic impulses propagating in different directions andcausing 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 occurswhen the atrial cells cannot repolarize in time for the nextincoming stimulus. Atrial fibrillation is characterized onthe ECG by a grossly disorganized pattern of atrial electri-cal activity that is irregular with respect to rate and rhythmand 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 randomoscillation of the baseline. Because of the random con-duction through the AV node, QRS complexes appear inan irregular pattern.

Atrial fibrillation is the only common arrhythmia inwhich the ventricular rate is rapid and the rhythm irregu-lar.34 The atrial rate typically ranges from 400 to 600 beatsper minute, with many impulses blocked at the AV node.The ventricular response is completely irregular, rangingfrom 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 apicalrate and the palpable peripheral pulses is called the pulsedeficit. The pulse deficit may increase when the ventricu-lar rate is high.

Atrial fibrillation may appear paroxysmally or as achronic phenomenon.31 It can be seen in persons withoutany apparent disease, or it may occur in individuals withcoronary artery disease, mitral valve disease, ischemic heartdisease, hypertension, myocardial infarction, pericarditis,congestive heart failure, digitalis toxicity, and hyperthy-roidism. Spontaneous conversion to sinus rhythm within24 hours of atrial fibrillation is common, occurring in up totwo thirds of persons with the disorder.33 Once the durationexceeds 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 increaseswith age. The incidence of chronic atrial fibrillation dou-bles with each decade of life and ranges from 2 or 3 newcases per 1000 population per year between the ages of 55and 64 years, to 35 new cases per 1000 per year betweenthe ages of 85 and 95 years.33

The symptoms of chronic atrial fibrillation vary. Somepeople have minimal symptoms, and others have severesymptoms, particularly at the onset of the arrhythmia.The symptoms may range from palpitations to acute pul-monary edema. Fatigue and other nonspecific symptomsare common in the elderly. The condition predisposesindividuals to thrombus formation in the atria, with sub-sequent risk for embolic stroke.

The treatment of atrial fibrillation is dependent on itscause, 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 withpersistent atrial fibrillation.33,34 Cardioversion may be con-sidered in some persons, particularly those with pulmonaryedema or unstable cardiac status. Because conversion tosinus rhythm is associated with increased risk for thrombo-embolism, anticoagulation therapy is usually administeredfor at least 3 weeks before cardioversion is attempted in per-sons in whom the duration of atrial fibrillation is unknownor exceeds 2 to 3 days.33 Transesophageal echocardiographycan be used to detect atrial thrombus, and transesophagealecho-guided cardioversion provides a means of ensuringthat atrial thrombus is not present when cardioversion isattempted. Anticoagulant medication is usually continuedafter cardioversion.

Junctional ArrhythmiasThe AV node can act as a pacemaker in the event the SAnode fails to initiate an impulse. Junctional rhythms canbe transient or permanent, and they usually have a rate of40 to 60 beats per minute. Junctional fibers in the AVnode or bundle of His also can serve as ectopic pacemak-ers, producing premature junctional complexes. Anotherrhythm originating in the junctional tissues is nonparox-ysmal junctional tachycardia. This rhythm usually is of


gradual onset and termination. However, it may occurabruptly if the dominant pacemaker slows sufficiently.The rate associated with junctional tachycardia rangesfrom 70 to 130 beats per minute, but it may be faster.1 TheP waves may precede, be buried in, or follow the QRScomplexes, 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 totreat some individuals with recurrent or intractable junc-tional tachycardia. Nonparoxysmal junctional tachycardiais observed most frequently in individuals with underlyingheart disease, such as inferior wall myocardial infarctionor myocarditis, or after open-heart surgery. It also may bepresent in persons with digitalis toxicity.

Disorders of Ventricular Conduction and RhythmThe junctional fibers in the AV node join with the bundleof His, which divides to form the right and left bundlebranches. The bundle branches continue to divide and formthe Purkinje fibers, which supply the walls of the ventricles(see Fig. 27-1). As the cardiac impulse leaves the junctionalfibers, it travels through the AV bundle. Next, the impulsemoves down the right and left bundle branches that lie be-neath the endocardium on either side of the septum. It thenspreads out through the walls of the ventricles. Interruptionof impulse conduction through the bundle branches iscalled bundle branch block. These blocks usually do not causealterations 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 afterthe other because the impulses must travel through muscletissue rather than through the specialized conduction tis-sue.35 This prolonged conduction causes the QRS complexto be wider than the normal 0.04 to 0.10 second. The leftbundle branch bifurcates into the left anterior and posteriorfascicles. An interruption of one of these fascicles is referredto as a hemiblock.

Long QT Syndrome and Torsades de PointesThe 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 calledtorsades de pointes and sudden cardiac death.36–38 Torsadesde pointes (twisting or rotating around a point) is a spe-cific type of ventricular tachycardia (Fig. 27-11). The termrefers to the polarity of the QRS complex, which swingsfrom positive to negative and vice versa. The QRS ab-normality is characterized by large, bizarre, polymorphic,

multiformed QRS complexes that vary, often from beat tobeat, in amplitude and direction, at, as well as in, rotationof the complexes around the isoelectric line. The rate oftachycardia is 100 to 180 beats per minute but can be asfast as 200 to 300 beats per minute. The rhythm is highlyunstable and may terminate in ventricular fibrillation orrevert to sinus rhythm.

LQTS is caused by various agents and conditions thatreduce the magnitude of outward repolarizing potassiumcurrents, enhance the magnitude of the inward depolariz-ing sodium and calcium currents, or both. Thus, there isdelayed repolarization of the ventricles with developmentof early depolarizing afterpotentials that initiate the ar-rhythmia. Typically, the QT interval is measured in a leadin 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 istypically corrected for heart rate and is noted as QTc.39–42

Nonetheless, a QTc greater than 440 msec in men andgreater than 460 msec in women has been linked withepisodes of sudden arrhythmia death syndrome. In addi-tion, T-wave morphology frequently is abnormal in patientswith LQTS.1,43

LQTS has been classified into hereditary and acquiredforms, both of which are associated with the developmentof torsades de pointes and sudden cardiac death. Thehereditary 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, thedisorder may result from a gene defect that alters the func-tion of a single ion channel. The gene mutations thatresult in congenital LQTS have been identified on chro-mosomes 3, 4, 7, 11, and 21.44 The hereditary forms ofLQTS are typically considered adrenergic dependent be-cause they are generally triggered by increased activity ofthe 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 virusHIV infection, and protein-sparing fasting.36,37,38,45 Med-ications linked to LQTS include digitalis, antiarrhythmicagents (e.g., amiodarone, procainamide, and quinidine),verapamil (calcium channel blocker), haloperidol (anti-psychotic agent), and erythromycin (antibiotic).37 Theacquired 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 formsof LQTS is primarily directed at identifying and withdraw-ing the offending agent, although emergency-type mea-sures that modulate the function of transmembrane ioncurrents can be lifesaving.

Ventricular ArrhythmiasArrhythmias that arise in the ventricles commonly areconsidered more serious than those that arise in the atriabecause they afford the potential for interfering with thepumping action of the heart.


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)

Premature Ventricular Contractions. A premature ven-tricular contraction (PVC) is caused by a ventricular ectopicpacemaker. After a PVC, the ventricle usually is unable torepolarize sufficiently to respond to the next impulse thatarises in the SA node. This delay is commonly referred to asa compensatory pause, which occurs while the ventriclewaits to reestablish its previous rhythm (Fig. 27-12). Whena PVC occurs, the diastolic volume usually is insufficientfor ejection of blood into the arterial system. As a result,PVCs usually do not produce a palpable pulse, or the pulseamplitude is significantly diminished. In the absence ofheart disease, PVCs typically are not clinically significant.The incidence of PVCs is greatest with ischemia, acutemyocardial infarction, history of myocardial infarction,ventricular hypertrophy, infection, increased sympatheticnervous system activity, or increased heart rate.46 PVCs alsocan be the result of electrolyte disturbances or medications.

A special pattern of PVC called ventricular bigeminy is acondition in which each normal beat is followed by orpaired with a PVC. This pattern often is an indication ofdigitalis toxicity or heart disease. The occurrence of fre-quent PVCs in the diseased heart predisposes the patient tothe development of other, more serious arrhythmias, in-cluding ventricular tachycardia and ventricular fibrillation.

Ventricular Tachycardia. Ventricular tachycardia describesa cardiac rhythm originating distal to the bifurcation ofthe bundle of His, in the specialized conduction system inventricular muscle, or both.1 It is characterized by a ven-

tricular rate of 70 to 250 beats per minute, and the onsetcan be sudden or insidious. Usually, ventricular tachy-cardia is exhibited electrocardiographically by wide, tall,bizarre-looking QRS complexes that persist longer than0.10 second (see Fig. 27-12). QRS complexes can be uniformin appearance, or they can vary randomly, in a repetitivemanner (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 morethan 30 seconds and requiring intervention, or it can benonsustained and stop spontaneously. This rhythm is dan-gerous because it eliminates atrial kick and can cause areduction in diastolic filling time to the point at which car-diac output is severely diminished or nonexistent.

Ventricular Flutter and Fibrillation. These arrhythmiasrepresent severe derangements of cardiac rhythm that ter-minate fatally within minutes unless corrective measuresare taken promptly. The ECG pattern in ventricular flutterhas 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. Theclassic ECG pattern of ventricular fibrillation is that ofgross disorganization without identifiable waveforms orintervals (see Fig. 27-12). When the ventricles do not con-tract, there is no cardiac output, and there are no palpableor audible pulses. The immediate defibrillation using anonsynchronized DC electrical shock is mandatory forventricular fibrillation and for ventricular flutter that hascaused loss of consciousness.28

Disorders of Atrioventricular ConductionUnder normal conditions, the AV junction, which consistsof the AV node with its connections to the entering atrialinternodal 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 atrialand ventricular conduction systems. Junctional fibers inthe AV node have high-resistance characteristics that causea delay in the transmission of impulses from the atria tothe ventricles. This delay provides optimal timing for atrialcontribution 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 commonlyassociated with fibrosis or scar tissue in fibers of the con-duction system. Conduction defects also may result frommedications, including digoxin, β-adrenergic–blockingagents, calcium channel–blocking agents, and class 1Aantiarrhythmic agents.47 Additional contributing factorsinclude electrolyte imbalances, inflammatory disease, orcardiac 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 theAV bundle (i.e., bundle of His), which is continuous withthe Purkinje conduction system that supplies the ventri-cles. The PR interval on the ECG corresponds with thetime it takes for the cardiac impulse to travel from the SAnode to the ventricular pathways. Normally, the PR inter-val ranges from 0.12 to 0.20 second.


Prematureventricular

contractions(PVC)

PVC PVC

Normal beats

Ventriculartachycardia

Ventricularfibrillation

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 thesinoatrial node, a PVC frequently is followed by a compensatorypause. Ventricular tachycardia (middle tracing) is characterized by arapid ventricular rate of 70 to 250 beats per minute and the ab-sence of P waves. In ventricular fibrillation (bottom tracing), there areno regular or effective ventricular contractions, and the ECG tracingis totally disorganized.

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 delayedAV conduction, but all atrial impulses are conducted to theventricles. This condition usually produces a regular atrialand ventricular rhythm. Clinically significant PR intervalprolongation can result from conduction delays in the AVnode itself, the His-Purkinje system, or both.1 When theQRS complex is normal in contour and duration, the AVdelay almost always occurs in the AV node and rarely inthe bundle of His. In contrast, when the QRS complex isprolonged, showing a bundle branch block pattern, con-duction delays may be in the AV node or the His-Purkinjesystem. First-degree block may be the result of disease inthe AV node such as ischemia or infarction, or of infec-tions such as rheumatic fever or myocarditis.48–50 Isolatedfirst-degree heart block usually is not symptomatic, andtemporary 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 ormore 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 thatconducted P waves relate to QRS complexes with recurringPR intervals; that is, the association of P waves with QRScomplexes is not random.1 Second-degree AV block hasbeen divided into two types: type I (i.e., Mobitz type I orWenckebach’s phenomenon) and type II (i.e., Mobitztype II). A Mobitz type I AV block is characterized by pro-

gressive lengthening of the PR interval until an impulse isblocked and the sequence begins again. It frequently occursin persons with inferior wall myocardial infarction, partic-ularly with concomitant right ventricular infarction.1 Thecondition usually is associated with an adequate ventricu-lar rate and rarely is symptomatic. It usually is transient anddoes not require temporary pacing. 27 In the Mobitz type IIAV 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 isassociated with a high mortality rate. In addition, Mobitztype II AV block is associated with other types of organicheart disease and often progresses to complete heart block.

Third-Degree AV Block. Third-degree, or complete, AVblock occurs when the conduction link for all impulsesfrom the SA node and atria through the AV node isblocked, 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 justbelow the region of the block. The atria usually continueto beat at a normal rate, and the ventricles develop theirown rate, which normally is slow (30 to 40 beats perminute). The atrial and ventricular rates are regular butdissociated. Third-degree AV block can result from aninterruption at the level of the AV node, in the bundle ofHis, or in the Purkinje system. Third-degree blocks at thelevel of the AV node usually are congenital, whereas blocksin the Purkinje system usually are acquired. Normal QRScomplexes, with rates ranging from 40 to 60 complexesper minute, usually are displayed on the ECG when theblock occurs proximal to the bundle of His.

Complete heart block causes a decrease in cardiac out-put with possible periods of syncope (fainting), known asa Stokes-Adams attack.1 Other symptoms include dizziness,fatigue, exercise intolerance, or episodes of acute heartfailure. Most persons with complete heart block require apermanent cardiac pacemaker.

DIAGNOSTIC METHODS

The diagnosis of disorders of cardiac rhythm and conduc-tion usually is made on the basis of the surface ECG. Furtherclarification of conduction defects and cardiac arrhythmiascan be obtained using electrophysiologic studies.

A resting surface ECG records the impulses originatingin the heart as they are recorded at the body surface. Theseimpulses 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 mayresult in iatrogenic heart disease.3 The resting ECG is thefirst approach to the clinical diagnosis of disorders of car-diac rhythm and conduction but it is limited to eventsthat occur during the period the ECG is being monitored.

Signal-Averaged ElectrocardiogramSignal-averaged ECG is a special type of ECG that is used todetect ventricular late action potentials that are thought to


AV block1st degree

PR= 0.38 sec.

AV block2nd degree

AV block3rd degree

QRS

P

P P T P P P PT P P TP

T P P T P P

QRS QRS QRS

QRS QRS

FIGURE 27-13 Electrocardiographic changes that occur with alter-ations in atrioventricular (AV) node conduction. The top tracingshows the prolongation of the PR interval, which is characteristic offirst-degree AV block. The middle tracing illustrates Mobitz type IIsecond-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.

originate from slow-conducting areas of the myocardium.Ventricular late action potentials are low-amplitude, high-frequency waveforms in the terminal QRS complex, andthey 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 cardiacdeath. These late potentials are detectable from leads ofthe surface ECG when signal averaging is performed.

The intent of signal averaging is reduction of noisethat makes surface ECG analysis more difficult to inter-pret. This technique averages together multiple samples ofQRS waveforms and creates a tracing that is an average ofall the repetitive signals. Signal averaging can be carriedout by using either temporal or spatial averaging. Both ap-proaches are based on the assumption that the noise israndom and that the signal of interest is coherent andrepetitive. 52 As a result, when several inputs that representthe same event are combined, the coherent signal will bereinforced, and the noise will cancel itself.

Temporal averaging is frequently referred to as signalaveraging. Most studies use temporal averaging as opposedto spatial averaging because it affords greater noise reduc-tion. Six standard bipolar orthogonal leads and one groundare typically used over a large number of beats (generally100 or more). Theoretically, this method allows for noisereduction by a factor of 10 or more.52 The implicit assump-tion underlying signal averaging is that the waveform isrepetitive and can be captured without loss of beat-to-beatsynchronization.

Spatial averaging uses from 4 to 16 electrodes,53 andthe 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 spacedelectrodes will respond to a common noise source and notcancel effectively, and the theoretical limit of a two-fold tofour-fold reduction in noise.52 The advantage of using spa-tial averaging is that it enhances one’s ability to provide asignal-averaged ECG from a single beat, thereby permit-ting beat-to-beat analysis of transient events and complexarrhythmias.

Signal averaging is a computer-based process. Eachelectrode 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 waveformto digital numbers that become a computer-readable ECG.

Holter MonitoringHolter monitoring is one form of long-term monitoringduring which a person wears a device that digitally recordstwo or three ECG leads for up to 48 hours. During thistime, the person keeps a diary of his or her activities orsymptoms, 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 experiencessymptoms, which assists the technician or physician incorrelating the diary, symptoms, and ECG changes dur-ing analysis. Holter monitoring is useful for documentingarrhythmias, conduction abnormalities, and ST-segmentchanges. The interpretative accuracy of long-term Holter

recordings varies with the system used and clinician ex-pertise. Most computer software packages used to scanHolter recordings are sufficiently accurate to meet clinicaldemand. The majority of patients who have ischemic heartdisease 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 antiarrhythmicdrug efficacy, episodes of myocardial ischemia, and heartrate variability.

Intermittent ECG recorders also are used in the diag-nosis of arrhythmias and conduction defects. There aretwo basic types of recorders that perform this type of mon-itoring.56 The first continuously monitors rhythm and isprogrammed to recognize abnormalities. In the second va-riety, the unit does not continuously monitor the ECGand therefore cannot automatically recognize abnormali-ties. This latter form relies on the person to activate theunit when he or she is symptomatic. The data are stored inmemory or transmitted telephonically to an electrocardio-graphic receiver, where they are recorded. These types ofECG recordings are useful in persons who have transientsymptoms.

Exercise Stress TestingThe exercise stress test elicits the body’s response to mea-sured increases in acute exercise (see Chapter 26). Thistechnique provides information about changes in heartrate, blood pressure, respiration, and perceived level of ex-ercise. It is useful in determining exercise-induced alter-ations in hemodynamic response and ischemic-type ECGST-segment changes, and it can detect and classify distur-bances in cardiac rhythm and conduction associated withexercise. These changes are indicative of a poorer prog-nosis in persons with known coronary disease and recentmyocardial infarction.

Electrophysiologic StudiesAn electrophysiologic study involves the passage of two ormore electrode catheters into the right side of the heart.These catheters are inserted into the femoral, subclavian,internal jugular, or antecubital veins and positioned withfluoroscopy into the high right atrium near the sinusnode, the area of the His bundle, the coronary sinus thatlies in the posterior AV groove, and into the right ventri-cle.7 The electrode catheters are used to stimulate the heartand record intracardiac ECGs. During the study, overdrivepacing, cardioversion, or defibrillation may be necessaryto terminate tachycardia induced during the stimulationprocedures.

Electrophysiologic studies are performed for diagnos-tic or therapeutic purposes. A diagnostic study is performedto determine a person’s potential for arrhythmia forma-tion. Electrophysiologic testing also defines reproduciblearrhythmia induction characteristics and, as a result, canbe used to evaluate the therapeutic efficacy of a particulartreatment 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 ofelectrophysiologic testing may be done repeatedly to testpatient responses to drugs, devices such as implantable de-fibrillators, and surgical interventions used in the treat-ment of arrhythmias.

Risks associated with electrophysiologic studies aresmall.57 Most electrophysiologic studies do not involveleft-sided heart access, and therefore the risk for myocar-dial infarction, stroke, or systemic embolism is less thanobserved with coronary arteriography. The addition oftherapeutic maneuvers, such as ablation therapy, to theprocedure increases the risk for complications.58 Predictorsof major complications include an ejection fraction of lessthan 35% and multiple ablation targets.59

QT DispersionA hallmark of reentrant arrhythmias is heterogeneity in re-fractoriness and conduction velocity. An index of theheterogeneity of ventricular refractoriness is found by ex-amining the differences in the length of QT intervals usingthe surface ECG. The most common index used to exam-ine QT dispersion is the difference between the longestand shortest QTc interval on the 12-lead ECG. Unusuallyhigh QT dispersion has been associated with the risk forlife-threatening arrhythmias in a variety of disorders,60 butthese results have been inconsistent.61,62 Many differenttechniques exist for determining QT dispersion, often mak-ing it difficult to compare results of various studies. Theutility of QT dispersion is not established as yet.28

TREATMENT

The treatment of cardiac rhythm or conduction disorders isdirected toward controlling the arrhythmia, correcting thecause, 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 drugtherapy, electrical stimulation, or surgical intervention.

Pharmacologic TreatmentAntiarrhythmic drugs act by modifying disordered forma-tion and conduction of impulses that induce cardiac mus-cle contraction. These drugs are classified into four majorgroups according to the drug’s effect on the action poten-tial of the cardiac cells. Although drugs in one categoryhave 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, andautomaticity to various degrees and therefore have been di-vided further into three groups: IA, IB, and IC. Class IAdrugs (e.g., quinidine, procainamide, disopyramide) de-crease automaticity by depressing phase 4 of the action po-tential, decrease conductivity by moderately prolongingphase 0, and prolong repolarization by extending phase 3of the action potential. Because these drugs are effective insuppressing ectopic foci and in treating reentrant arrhyth-

mias, they are used for supraventricular and ventriculararrhythmias. Class IB drugs (e.g., lidocaine, phenytoin, me-xiletine) decrease automaticity by depressing phase 4 of theaction potential, have little effect on conductivity, decreaserefractoriness by decreasing phase 2, and shorten repolar-ization by decreasing phase 3. Drugs in this group are usedfor treating ventricular arrhythmias only and have littleor 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 ventriculararrhythmias 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 effectof sympathetic nervous system stimulation on the heart.These drugs decrease automaticity by depressing phase 4of the action potential; they also decrease heart rate andcardiac contractility. These medications are effective fortreatment 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 agentsreduce the force of myocardial contractility, thereby de-creasing myocardial oxygen demand. These drugs are usedto slow the ventricular response in atrial tachycardias and toterminate reentrant paroxysmal supraventricular tachycar-dias when the AV node functions as a reentrant pathway.28

Two other types of antiarrhythmic drugs, the cardiacglycosides 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 atrialfibrillation. Adenosine, an endogenous nucleoside that ispresent in every cell, is used for emergency intravenoustreatment of paroxysmal supraventricular tachycardia in-volving the AV node. It interrupts AV node conduction andslows SA node firing.

Electrical InterventionsThe correction of conduction defects, bradycardias, andtachycardias 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 backmore than a century. During this time, tremendous strideshave been made in the effectiveness of cardiac pacing. Acardiac pacemaker is an electronic device that delivers anelectrical stimulus to the heart. It is used to initiate heart-beats in situations in which the normal pacemaker of the


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 toperfuse vital tissues, as well as other cardiac arrhythmias.A pacemaker may be used as a temporary or a permanentmeasure. Pacemakers can pace the atria, the ventricles, orthe atria and ventricles sequentially, or overdrive pacingcan be used. Overdrive pacing is used to treat recurrentventricular tachycardia and reentrant atrial or ventriculartachyarrhythmias, and to terminate atrial flutter.

Temporary pacemakers are useful for treatment ofsymptomatic bradycardias and to perform overdrive pac-ing. They can be placed transcutaneously, transvenously,or epicardially. External temporary pacing, also known astranscutaneous pacing, involves the placement of large patchelectrodes on the anterior and posterior chest wall, whichthen are connected by a cable to an external pulse gener-ator. Many defibrillators today have transcutaneous pac-ing capabilities as well. Internal temporary pacing, alsoknown as transvenous pacing, involves the passage of a ve-nous catheter with electrodes on its tip into the rightatrium or ventricle, where it is wedged against the endo-cardium. The electrode then is attached to an external pulsegenerator. This procedure is performed under fluoroscopicor electrocardiographic direction. During open thoracot-omy procedures, epicardial pacing wires sometimes areplaced. These wires are brought out directly through thechest wall and also can be attached to an external pulse gen-erator, if necessary.

Permanent cardiac pacemakers may become necessaryfor a variety of reasons. Permanent pacemakers require im-plantation of pacing wires into the epicardium and a pulsegenerator. The pulse generator typically weighs approxi-mately 25 to 40 g.64 Ongoing evaluation of the pacemaker’ssensing and firing capabilities is necessary.

Synchronized cardioversion is used to terminate tachy-cardias due to reentry, such as atrial fibrillation and mostforms of ventricular tachycardia, and defibrillation is usedas a life-saving intervention in ventricular fibrillation. Thedischarge of electrical energy that is synchronized with theR 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 heartcompletely during passage of the current. This electrical cur-rent interrupts the disorganized impulses, allowing the SAnode to regain control of the heart. Defibrillation and syn-chronized cardioversion can be delivered externally throughlarge patch electrodes on the chest or internally throughsmall paddle electrodes placed directly on the myocardium,patch electrodes sewn into the epicardium, or transvenouswires placed in the right ventricle. Electrical devices thatcombine antitachycardial pacing, cardioversion, defibril-lation, and bradycardial pacing are under investigation.

Automatic implantable cardioverter-defibrillators(AICDs) are being used successfully to treat individualswith life-threatening ventricular tachyarrhythmias by theuse 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 frameprovides nearly a 100% likelihood of reversal of the ar-rhythmia, supporting the utility of this device as a reliableand effective means of preventing sudden cardiac death insurvivors of out-of-hospital cardiac arrest.

Ablation and Surgical InterventionsAblation therapy is used for treating recurrent, life-threat-ening supraventricular and ventricular tachyarrhythmias.It involves localized destruction, isolation, or excision ofcardiac tissue that is considered to be arrhythmogenic.7,28

Ablative therapy may be performed by catheter or surgicaltechniques. Radiofrequency ablation uses radiofrequencyenergy waves to destroy defective or aberrant electricalconduction pathways. Cryoablation is the direct applica-tion of an extremely cold probe to arrhythmogenic cardiactissue that causes freezing and necrosis of defective or aber-rant electrical conduction pathways. The major complica-tion with surgical ablation techniques is the perioperativemortality rate of 5% to 15%.7 There also has been a highmorbidity rate reported.

Additional surgical interventions such as coronaryartery bypass surgery, ventriculotomy, and endocardial re-section may be used to improve myocardial oxygenation,remove arrhythmogenic foci, or alter electrical conductionpathways. Coronary artery bypass surgery improves myo-cardial oxygenation by increasing blood supply to themyocardium. Ventriculotomy involves the removal ofaneurysm tissue and the resuturing of the myocardial wallsto eliminate the paradoxical ventricular movement and thefoci of arrhythmias. In endocardial resection, endocardialtissue that has been identified as arrhythmogenic throughthe use of electrophysiologic testing or intraoperative map-ping is surgically removed. Ventriculotomy and endocar-dial resection have been performed with cryoablation orlaser ablation as an adjunctive therapy.28 Other surgicaltechniques, including transvenous electrocoagulation66 andlaser ablation,67 are under investigation as potential treat-ment modalities for recurrent tachycardias.

In summary, disorders of cardiac rhythm arise as the resultof disturbances in impulse generation or conduction in theheart. 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. Cardiacarrhythmias are not necessarily pathologic; they occur inhealthy and diseased hearts. Sinus arrhythmias originate in theSA node. They include sinus bradycardia (heart rate <60 beatsper minute); sinus tachycardia (heart rate >100 beats perminute); sinus arrest, in which there are prolonged periods ofasystole; and sick sinus syndrome, a condition characterized byperiods of bradycardia alternating with tachycardia.

Atrial arrhythmias arise from alterations in impulse gener-ation that occur in the conduction pathways or muscle of theatria. 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). Atrialarrhythmias often go unnoticed unless they are transmitted tothe ventricles.

Arrhythmias that arise in the ventricles commonly are con-sidered more serious than those that arise in the atria becausethey 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 pointesand sudden cardiac death. PVCs are caused by a ventricularectopic pacemaker. Ventricular tachycardia is characterized bya ventricular rate of 70 to 250 beats per minute. Ventricular fib-rillation (e.g., ventricular rate >350 beats per minute) is a fatalarrhythmia unless it is successfully treated with defibrillation.

Alterations in the conduction of impulses through the AVnode lead to disturbances in the transmission of impulses fromthe atria to the ventricles. There can be a delay in transmission(i.e., first-degree heart block), failure to conduct one or moreimpulses (i.e., second-degree heart block), or complete failureto conduct impulses between the atria and the ventricles (i.e., third-degree heart block). Conduction disorders of thebundle of His and Purkinje system, called bundle branch blocks,cause a widening of and changes in the configuration of theQRS complex of the ECG.

The diagnosis of disorders of cardiac rhythm and conduc-tion typically is accomplished using surface ECG recordings orelectrophysiologic studies. Surface electrodes can be used toobtain a 12-lead ECG; signal-averaged electrocardiographicstudies in which multiple samples of QRS waves are averagedto 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 ameans of directly stimulating the heart while obtaining anintracardiac ECG recording.

Both electrical devices and medications are used in thetreatment of arrhythmias and conduction disorders. Tempo-rary and permanent cardiac pacemakers are used to treatsymptomatic bradycardias or to provide overdrive pacing pro-cedures. Defibrillation is used to treat ventricular fibrillation.Synchronized cardioversion procedures are carried out to treatatrial 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 heartcompletely, supplying the SA node with an opportunity to takeover as the primary pacemaker of the heart. Radiofrequencyablation and cryoablation therapy are used to destroy specificirritable foci in the heart. Surgical procedures can be performedto 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 heartfailure comes to the clinic complaining of feeling tired.Her heart rate is 97 beats per minute, and the rhythm isirregularly irregular.

A. What type of arrhythmia do you think she might behaving? 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 ofarrhythmia?

A 42-year-old man appears at the urgent care center withcomplaints of chest discomfort, shortness of breath, andgenerally not feeling well. You assess vital signs and findthat he has a temperature of 99.2°F, blood pressure of166/90 mm HG, pulse of 87 beats per minute andslightly irregular, and respiratory rate of 26 breaths perminute. 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 hisunderlying rhythm is normal sinus rhythm, but heis having frequent premature contractions that aremore than 0.10 sec in duration. You suspect thatthese 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 thisman?

D. What do you think the etiology of this arrhythmiamight be? How might it be treated?

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Conduction of Heart