1882 PART 6 Disorders of the Cardiovascular System

First-degree AV block

Fixed PR prolongation

Second-degree Mobitz I (Wenckebach) AV block

Progressive prolongation of PR interval followed by a nonconduct P wave

Second-degree Type II AV block

Fixed PR interval prior to a

nonconducted P wave

N N h h

v1

v

v3

v

v

Complete (third-degree) AV block

AV dissociation with ventricular rate slower than atrial rate

FIGURE 245-1 Types of atrioventricular (AV) block. The upper left figure displays fixed prolongation of the PR interval. The upper right figure demonstrates Mobitz I block

(Wenckebach AV block) manifested as progressive prolongation of the PR interval followed by a nonconducted P wave (“dropped beat”). The lower left figure displays AV

block with P wave with no QRS complex and no associated PR prolongation prior to the dropped beat (Mobitz type II AV block). The lower right figure demonstrates complete

heart block manifested as dissociation between P waves and QRS complexes (AV dissociation).

TABLE 245-2 Causes of AV Block

Fibrosis/sclerosis/calcification of the conduction system

Senile degeneration of the conduction system (Lev’s disease)

Lenègre’s disease

Calcification of the aortic valve annulus (mitral—less common)

Iatrogenic

After cardiac surgery (including valve surgery)

TAVR/alcohol septal ablation

Complication from catheter ablation

Medication (beta blockers, verapamil, diltiazem, digoxin)

Toxin/overdose/poisoning

Acute MI/coronary ischemia

Infectious causes

Lyme carditis

Bacterial endocarditis with perivalvular abscess

Viral myocarditis

Chagas’ disease

Toxoplasmosis

Infiltrative heart disease/inflammatory disease

Sarcoidosis

Amyloid

 Rheumatologic disease: reactive arthritis (Reiter’s syndrome), SLE, RA,

systemic sclerosis

Congenital AV block

Maternal lupus

Idiopathic congenital AV block

Congenital heart defects

Genetic

Endocrine (e.g., thyroid disease, hypoadosteronism)

Autoimmune disease

Neuromuscular disease (e.g., myotonic dystrophy, Kearns-Sayre syndrome, Erb’s

dystrophy)

Lymphoma

Enhanced vagal tone/neurocardiogenic

Abbreviations: AV, atrioventricular; MI, myocardial infarction; RA, rheumatoid

arthritis; SLE, systemic lupus erythematosus; TAVR, transcatheter aortic valve

replacement.

unstable escape rhythms and a worse prognosis with high mortality

rates.

AV conduction abnormalities may be caused by either direct ischemia to the conduction system or enhanced autonomic tone (BezoldJarisch reflex). Conduction abnormalities can be considered based on

infarct location, and this may also predict which conduction abnormalities may be reversible. High-grade AV block associated with inferior

MI is often located proximal to the His bundle in 90% of patients.

Narrow junctional escape typically occurs with rates >40 beats/min,

and a temporary pacemaker is typically not required as the AV block

is often reversible and successfully managed with pharmacologic

therapy. High-grade AV block in the setting of anterior MI is typically

indicative of extensive infarction, is more often distal to the AV node,

and is associated with a high mortality rate. Temporary pacing in this

circumstance is typically indicated. CHB in the setting of anterior MI

may also be preceded by RBB block due to the arterial supply of the

proximal RBB.

■ INFECTIOUS CAUSES OF AV BLOCK

Infection can also cause AV block. AV block is a common manifestation of Lyme carditis due to infection with Borrelia burgdorferi. AV

block is typically at the level of the AV node with narrow junctional

escape rhythm >40 beats/min. Less commonly, conduction abnormalities can occur below the level of the AV node or in the sinus node. AV

block typically improves within 1 week of antibiotic therapy, although

a longer time frame can occur in some patients. AV block in the setting

of infective endocarditis should raise concern for perivalvular abscess,

which may necessitate surgical intervention. Viral myocarditis, Chagas’

disease, and toxoplasmosis are less common infectious causes of AV

block. Infiltrative heart disease such as cardiac sarcoid, amyloid, and

hemochromatosis can present as AV block. Autoimmune diseases,

including systemic lupus erythematosus (SLE), rheumatoid arthritis,

mixed connective tissue disease, and scleroderma, may cause AV block

due to infiltration of the conduction system. Rare malignancies also

may impair AV conduction.

■ AUTONOMIC AND FUNCTIONAL CAUSES OF AV

BLOCK

Functional causes of AV block (autonomic, metabolic/endocrine, and

drug-related) tend to be reversible. Most other etiologies produce

structural changes, typically fibrosis, in segments of the AV conduction

The Bradyarrhythmias: Disorders of the Atrioventricular Node

1883CHAPTER 245

400 ms

There is a slowing of the

sinus rate prior to AV block

AV block in the setting of

high vagal tone during sleep

30 s

17 mm/mV, 8 s

FIGURE 245-2 Evidence of atrioventricular (AV) block during sleep. During sleep, increased vagal tone leads to sinus bradycardia with associated Mobitz I (Wenckebach)

AV block. See Fig. 245-1 for an explanation of Mobitz I block.

axis that are generally permanent. Heightened vagal tone during sleep

or in well-conditioned individuals can be associated with all grades of

AV block (Fig. 245-2).

Carotid sinus hypersensitivity, vasovagal syncope, and cough and

micturition syncope may be associated with SA node slowing and

AV conduction block. Transient metabolic and endocrinologic disturbances and a number of pharmacologic agents also may produce

reversible AV conduction block.

■ ACQUIRED AV BLOCK FROM FIBROSIS AND

INFILTRATIVE CARDIOMYOPATHIES

Idiopathic progressive fibrosis of the conduction system is one of the

more common and degenerative causes of AV conduction block. Aging

is associated with degenerative changes in the summit of the ventricular septum, central fibrous body, and aortic and mitral annuli and has

been described as “sclerosis of the left cardiac skeleton.” The process

typically begins in the fourth decade of life and may be accelerated by

atherosclerosis, hypertension, and diabetes mellitus. Accelerated forms

of progressive familial heart block have been identified in families with

mutations in the cardiac sodium channel gene (SCN5A) and other loci

that have been mapped to chromosomes 1 and 19.

AV conduction block has been associated with heritable neuromuscular diseases, including the nucleotide repeat disease myotonic

dystrophy, the mitochondrial myopathy Kearns-Sayre syndrome, and

several of the monogenic muscular dystrophies.

■ CONGENITAL AV BLOCK

Congenital AV block may be observed in complex congenital cardiac

anomalies, such as transposition of the great arteries, ostium primum

ASDs, VSDs, endocardial cushion defects, and some single-ventricle

defects. Congenital AV block in the setting of a structurally normal

heart has been seen in children born to mothers with SLE and other

autoimmune diseases.

DIAGNOSTIC TESTING

Patients with conduction abnormalities should be evaluated for the

presence or absence of structural heart disease. Physical exam may

reveal valvular heart disease. ECG may suggest concomitant disease

that predisposes to conduction abnormalities. Echocardiography is

also indicated to evaluate for structural heart disease including valvular

abnormalities, ejection fraction, and ventricular wall motion. Because

age-dependent progressive fibrosis of the conduction system is the

most common cause, AV node block that develops at a younger age

(≤60 years) may warrant advanced imaging such as chest computed

tomography (CT), cardiac magnetic resonance imaging (MRI), or CT/

positron emission tomography (PET) scan to further evaluate for infiltrative heart disease such as sarcoidosis. Advanced imaging may also be

warranted based on other factors in the history and testing that suggest

the need for evaluation of infiltrative heart disease. Evaluation for cardiac ischemia should be driven by the clinical suspicion at presentation

(e.g., symptoms of ischemia, ECG abnormalities, etc.) (Fig. 245-3).

Diagnostic testing in the evaluation of AV block is aimed at determining the level of conduction block, particularly in asymptomatic

patients, since the prognosis and therapy depend on whether the block

is in or below the AV node. Vagal maneuvers, carotid sinus massage,

exercise, and administration of drugs such as atropine and isoproterenol may be diagnostically informative. Owing to the differences in the

innervation of the AV node and infranodal conduction system, vagal

stimulation and carotid sinus massage slow conduction in the AV node

but have less of an effect on infranodal tissue and may even appear to

improve conduction due to a reduced rate of activation of distal tissues.

Conversely, atropine, isoproterenol, and exercise improve conduction

through the AV node and may appear to impair infranodal conduction.

In patients with congenital CHB and a narrow QRS complex, exercise

typically increases heart rate; by contrast, those with acquired CHB,

particularly with wide QRS, do not respond to exercise with an increase

in heart rate.

Additional diagnostic evaluation, including electrophysiologic testing, may be indicated in patients with syncope and suspected highgrade AV block. This is particularly relevant if noninvasive testing

does not reveal the cause of syncope or if the patient has structural

heart disease with ventricular tachyarrhythmias as a cause of symptoms. Electrophysiologic testing provides more precise information

regarding the location of AV conduction block and permits studies of

AV conduction under conditions of pharmacologic stress and exercise.

Recording of the His bundle electrogram by a catheter positioned at the

superior margin of the tricuspid valve annulus provides information

about conduction at all levels of the AV conduction axis. A properly

recorded His bundle electrogram reveals local atrial activity, the His

electrogram, and local ventricular activation; when it is monitored

simultaneously with recorded body surface ECG traces, intra-atrial, AV

nodal, and infranodal conduction times can be assessed. The time from

the most rapid deflection of the atrial electrogram in the His bundle

recording to the His electrogram (AH interval) represents conduction

through the AV node and is normally <130 ms. The time from the His

electrogram to the earliest onset of the QRS on the surface ECG (HV

interval) represents the conduction time through the His-Purkinje

system and is normally ≤55 ms (Fig. 245-4).

Rate stress produced by pacing can unveil abnormal AV conduction.

Mobitz I second-degree AV block at short atrial paced cycle lengths is a

normal response. However, when it occurs at atrial cycle lengths >500 ms

(<120 beats/min) in the absence of high vagal tone, it is abnormal. Typically, type I second-degree AV block is associated with prolongation

of the AH interval, representing conduction slowing and block in the

AV node. AH prolongation occasionally is due to the effect of drugs

(beta blockers, calcium channel blockers, digitalis) or increased vagal

tone. Atropine can be used to reverse high vagal tone; however, if AH

prolongation and AV block at long pacing cycle lengths persist, intrinsic AV node disease is likely. Type II second-degree block is typically

infranodal, often in the His-Purkinje system. Block below the node

with prolongation of the HV interval or a His bundle electrogram with

no ventricular activation is abnormal unless it is elicited at fast pacing

rates or short coupling intervals with extra stimulation. It is often difficult to determine the type of second-degree AV block when 2:1 conduction is present; however, the finding of a His bundle electrogram

after every atrial electrogram indicates that block is occurring in the

distal conduction system.

Intracardiac recording at an electrophysiologic study that reveals

prolongation of conduction through the His-Purkinje system (i.e., long

1884 PART 6 Disorders of the Cardiovascular System

Evidence for AV

block

Reversible or

physiologic cause

Transthoracic

echocardiography

(Class I)

Transthoracic

echocardiography

(Class IIa)

Mobitz

type II 2nd AV block,

advanced AV block,

complete heart

block

Treatment

effective or not

necessary

Treat underlying cause as

needed, e.g., sleep apnea

(Class I)

Observe

Observe Observe

Symptoms Symptoms

Exercise testing

(Class IIa)

Electrophysiology

study

(Class IIb)

AV node

(Mobitz type I)

Determine

site of AV

block

Treat identified

abnormalities

Advanced

imaging*

(Class IIa)

Advanced

imaging*

(Class IIa)

AV node

Unclear

e.g., 2:1 AV block

Suspicion

for infiltrative CM,

endocarditis, ACHD,

etc. Suspicion

for infiltrative CM,

endocarditis, ACHD,

etc.

Suspicion

for structural heart

disease

AV block

treatment

algorithm

AV block

treatment

algorithm

AV block

treatment

algorithm

AV block

treatment

algorithm

AV block

treatment

algorithm

Yes

Yes

Yes

Yes

Yes

Yes Yes

Yes

No

No

No

No No

No No

No

Intranodal

Intranodal

Infranodal

FIGURE 245-3 Initial evaluation of suspected atrioventricular (AV) block algorithm. *Targeted advanced imaging—magnetic resonance imaging (MRI): amyloidosis,

myocarditis, hemochromatosis, sarcoidosis, congenital heart disease (CHD), sinus of Valsalva aneurysm, aortic dissection, arrhythmogenic right ventricular

cardiomyopathy; fluorodeoxyglucose-positron emission tomography (FDG-PET): sarcoidosis; technetium-99m pyrophosphate (Tc PYP) or 99m technetium 3,3-diphosphono1,2-propanodicarboxylic acid (TC-DPD): transthyretin (TTR) amyloidosis; cardiac computed tomography (CT): CHD, sinus of Valsalva. ACHD, adult CHD; CM, cardiomyopathy.

(Reproduced with permission from FM Kusumoto et al: 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction

delay. Heart Rhythm 16:e128, 2019.)

The Bradyarrhythmias: Disorders of the Atrioventricular Node

1885CHAPTER 245

I

II

III

V1

HI Sd

HI Sp

RVA

HRA

HA

H A

H A

H A

H A

H A

V

FIGURE 245-4 High-grade atrioventricular (AV) block below the His. The AH interval is normal and is not changing before the block. Atrial and His bundle electrograms

are recorded consistent with block below the distal AV junction. I, II, III, and V1

 are surface ECG leads. HISp, HISd, and RVA are the proximal HIS, distal HIS, and right

ventricular apical electrical recordings, respectively. A, H, and V represent the atrial, His, and ventricular electrograms on the His bundle recording, respectively. (Courtesy

of Dr. Joseph Marine.)

HV interval) is associated with an increased risk of progression to

higher grades of block and is generally an indication for pacing. In the

setting of bundle branch block, the HV interval may reveal the condition of the unblocked bundle and the prognosis for developing more

advanced AV conduction block. Prolongation of the HV interval in

patients with asymptomatic bundle branch block is associated with an

increased risk of developing higher-grade AV block. The risk increases

with greater prolongation of the HV interval such that in patients with

an HV interval >100 ms, the annual incidence of complete AV block

approaches 10%, indicating a need for pacing. In patients with acquired

CHB, even if intermittent, there is little role for electrophysiologic testing, and pacemaker implantation is almost always indicated.

TREATMENT

Acute Management of AV Conduction Block

The first-line strategies for management of AV block should be

to eliminate reversible causes and to determine the immediate

safety and reliability of the heart rhythm (e.g., escape rhythm) and

whether or not temporary or permanent pacing is warranted. The

need for temporary pacing is determined by the symptoms of the

patient, hemodynamic status, and the estimate of the level at which

AV block is present. In a general sense, the lower in the conduction

system that an escape rhythm is occurring, the lower is the reliability of the escape rhythm. A narrow-complex junctional escape of

45 beats/min with no symptoms does not warrant urgent temporary

pacing, whereas a wide-complex (implying block lower in the conduction system) escape rhythm at 30 beats/min does. Elimination

of unnecessary medications known to slow AV conduction (e.g.,

beta blockers, diltiazem, verapamil, digoxin), correction of electrolyte abnormalities, ischemia, and inhibition of excessive vagal tone

may increase the heart rate. Adjunctive pharmacologic treatment

with atropine or isoproterenol may be useful if the block is in the

AV node. When pacing is indicated, the most expeditious technique

is the use of transcutaneous pacing, where pacing patches are placed

anteriorly over the cardiac apex (cathode) and posteriorly between

the spine and the scapula or above the right nipple (anode). Acutely,

transcutaneous pacing is highly effective, but its duration is limited

by patient discomfort and longer-term failure to capture the ventricle owing to changes in lead impedance. Transvenous temporary

pacing is more reliable, and a pacing wire can be placed from the

jugular, subclavian, or femoral venous system and advanced to the

right ventricle, permitting stable temporary pacing.

AV conduction abnormalities may be reversible in certain circumstances including removal of unnecessary medication or toxins,

correction of electrolyte abnormalities, relief of ischemia, treatment

of certain infiltrative heart disease (e.g., immunosuppression in

cardiac sarcoidosis), and treatment of sleep apnea in patients with

nocturnal vagally mediated AV block. When symptomatic or infranodal AV block is not reversible, which is often the case, permanent

pacing is warranted.

PERMANENT PACEMAKER IMPLANTATION

The indications for pacing in AV conduction block are shown in

Fig. 245-5. In patients with acquired Mobitz type II AV block,

high-grade AV block, or third-degree AV block that is not reversible

or physiologic, permanent pacing is recommended regardless of

symptoms. For all other types of AV block, in the absence of conditions associated with progressive AV conduction abnormalities,

permanent pacing should generally be considered only in the presence of symptoms that correlate with block. In patients with neuromuscular disease and other progressive cardiomyopathies affecting

the conduction system, permanent pacemaker implantation is recommended for marked first-degree AV block and Mobitz I AV

block. Pacemaker implantation should be performed in any patient

1886 PART 6 Disorders of the Cardiovascular System

with symptomatic bradycardia and irreversible second- or thirddegree AV block, regardless of the cause or level of block in the

conducting system. Symptoms may include those directly related to

bradycardia and low cardiac output or to worsening heart failure,

angina, or intolerance to an essential medication. Pacing in patients

with asymptomatic AV block should be individualized; situations in

which pacing should be considered are patients with acquired CHB,

particularly in the setting of cardiac enlargement; left ventricular

dysfunction; and waking heart rates ≤40 beats/min. Patients who

have asymptomatic second-degree AV block of either type should

be considered for pacing if the block is demonstrated to be intra- or

infra-His or is associated with a wide QRS complex. Pacing may

be indicated in asymptomatic patients in special circumstances, in

patients with profound first-degree AV block and left ventricular

dysfunction in whom a shorter AV interval produces hemodynamic

improvement, and in the setting of milder forms of AV conduction

delay (first-degree AV block, intraventricular conduction delay)

in patients with neuromuscular diseases that have a predilection

for the conduction system, such as myotonic dystrophy and other

muscular dystrophies and Kearns-Sayre syndrome.

AV block in acute MI is often transient, particularly in inferior

infarction. The circumstances in which pacing is indicated in acute

MI are persistent second- or third-degree AV block, particularly

if symptomatic, and transient second- or third-degree AV block

associated with bundle branch block. Pacing is generally not indicated in the setting of transient AV block in the absence of intraventricular conduction delays or in the presence of fascicular block

or first-degree AV block that develops in the setting of preexisting

bundle branch block. Fascicular blocks that develop in acute MI in

the absence of other forms of AV block also do not require pacing.

Distal forms of AV conduction block may require pacemaker

implantation in certain clinical settings. Patients with bifascicular

or trifascicular block and symptoms, particularly syncope that

is not attributable to other causes, should undergo pacemaker

implantation. Permanent pacemaker implantation is indicated in

asymptomatic patients with bifascicular or trifascicular block who

experience intermittent third-degree block, type II second-degree

AV block, or alternating bundle branch block. In patients with

fascicular block who are undergoing electrophysiologic study, a

markedly prolonged HV interval or block below the His at long

cycle lengths also may constitute an indication for permanent pacing. Patients with fascicular block and the neuromuscular diseases

previously described should also undergo pacemaker implantation.

SELECTION OF PACING MODE AND SYSTEM

In general, a pacing mode that maintains AV synchrony reduces

complications of pacing such as pacemaker syndrome and

pacemaker-mediated tachycardia. This is particularly true in

younger patients; the importance of dual-chamber pacing in the

elderly, however, is less well established, although AV synchrony in

patients with sinus rhythm and AV block is typically desired.

Physiologic Ventricular Pacing In patients with left ventricular

ejection fraction <50% and AV block who have an indication for

permanent pacing and are expected to require ventricular pacing

>40% of the time, techniques to provide more physiologic ventricular activation are preferred to right ventricular pacing to prevent

heart failure. Cardiac resynchronization therapy (CRT) involves

placement of an additional pacing lead in a lateral or anterolateral

branch of the coronary sinus to allow for simultaneous right ventricle and lateral left ventricle pacing leading to a more physiologic

left ventricular contraction. CRT pacing has been shown to improve

outcomes and mortality in appropriately selected patients. Physiologic ventricular pacing has also been achieved with placement

of a ventricular pacing lead in the region of the His bundle. His

bundle pacing recruits the specialized conduction system, leading

to a more physiologic cardiac contraction. In addition to His bundle pacing, left bundle branch area pacing in the proximal interventricular septal region has also been shown to achieve a more

Symptoms

Lamin A/C,

neuromuscular

disease

Neuromuscular

disease associated with

progressive conduction tissue

disorder

Complete heart

block (acquired),

advanced AV

block,

Mobitz Type II,

evidence for

infranodal block

Observation

Observation

Lamin

A/C

Neuromuscular

disease

Permanent

pacing

(Class IIa)

Permanent

pacing

(Class IIb)

Permanent

pacing

(Class IIa)

Permanent

pacing

(Class IIa)

Permanent

pacing

(Class I)

Permanent

pacing

(Class I)

Permanent

pacing

(Class III:

Harm)

Permanent

pacing

(Class III:

Harm)

Symptoms

Marked first degree AV Block Mobitz Type I Block

AV Block

Yes No Yes

Yes

No

No

Yes No

Yes Yes

No

FIGURE 245-5 Indications for pacing in patients with atrioventricular (AV) block. In patients presenting with AV block, the category of AV block should be determined

(first-degree, second-degree, or complete heart block). In first-degree AV block, permanent pacing may be indicated in the setting of symptoms or higher-risk systemic

disease such as neuromuscular disease or Lamin A/C cardiomyopathy. In Mobitz I AV block, pacing may be considered in the setting of symptoms or the additional

disease mentioned with first-degree AV block. In complete heart block or Mobitz II AV block, permanent pacing is generally indicated. Class I recommendations should be

performed or are indicated. Class IIa recommendations are considered reasonable to perform. Class IIb recommendations may be considered. Class III recommendations

are associated with harm more than benefit. (Reproduced with permission from FM Kusumoto et al: 2018 ACC/AHA/HRS guideline on the evaluation and management of

patients with bradycardia and cardiac conduction delay. Heart Rhythm 16:e128, 2019.)

The Bradyarrhythmias: Disorders of the Atrioventricular Node

1887CHAPTER 245

Pacing lead at

His position

FIGURE 245-6 His bundle pacing. The chest radiograph on the left shows a dual chamber pacemaker with a pacing lead in the right atrium (upper left) and a pacing lead

in the region of the tricuspid valve in the His position. The electrocardiograms demonstrated intrinsic conduction with complete heart block on the left and atrial sensed,

ventricular paced rhythm with a narrow QRS complex similar to the intrinsic QRS complex that results from pacing the His bundle and capturing the specialized conduction

system of the heart.

physiologic pacing response. The selection of pacing lead location

should be individualized (Fig. 245-6).

The availability of leadless miniaturized pacing systems may be

appropriate in selected patients. Leadless pacemakers are completely

self-contained devices that are implanted via the femoral vein into

the right ventricle. The technology for these devices continues to

evolve, and the most recent models are capable of detecting atrial

mechanical contraction to allow for the preservation of AV synchrony. The device can provide single-chamber ventricular pacing

in addition to containing technology that can sense atrial activity

(utilizing the accelerometer in the pacemaker) to coordinate an

atrial sensed, ventricular paced rhythm (AV synchrony). Leadless

pacemakers can be particularly useful in patients with vascular

access limitations. Because there is no intravascular pacing wire or

implanted subcutaneous pacemaker generator, the long-term infection rate is lower and there is no risk of lead fracture (Fig. 245-7).

Several studies have failed to demonstrate a difference in mortality rate in older patients with AV block treated with a single- (VVI)

compared with a dual- (DDD) chamber pacing mode. In some of

the studies that randomized pacing mode, the risk of chronic atrial

fibrillation and stroke risk decreased with physiologic pacing. In

patients with sinus rhythm and AV block, the very modest increase

in risk with dual-chamber pacemaker implantation appears to be

justified to avoid the possible complications of single-chamber

pacing.

Acknowledgment

David D. Spragg and Gordon F. Tomaselli contributed to this chapter in

the 20th edition, and some material from that chapter has been retained

here.

■ FURTHER READING

Ellenbogen K et al (eds): Clinical Cardiac Pacing, Defibrillation, and

Resynchronization Therapy, 5th ed. Philadelphia, Elsevier, 2016.

Jalife J, Stevenson W (eds): Zipes and Jalife’s Cardiac Electrophysiology: From Cell to Bedside, 8th ed. Philadelphia, Elsevier, 2021.

Kusumoto FM et al: 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac

conduction delay: A report of the American College of Cardiology/

American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm 16:e128, 2019.

Single chamber transvenous pacemaker Single chamber leadless pacemaker

FIGURE 245-7 Types of pacemakers. A single-chamber pacemaker with the pacing lead in the right ventricular outflow tract (arrow) is shown on the left. A single-chamber

leadless pacemaker (arrow) is shown on the right.

1888 PART 6 Disorders of the Cardiovascular System

The most common arrhythmias that patients present with are part of

a broad category defined by anatomic origin termed supraventricular

tachycardias (SVTs). SVTs originate from or are dependent on conduction through the atrium or atrioventricular (AV) node to the ventricles.

Most produce narrow QRS complex tachycardia (QRS duration <120 ms)

characteristic of ventricular activation over the Purkinje system and

thus are sometimes referred to as a narrow-complex tachycardias. The

QRS morphology of the SVT is usually identical to the sinus rhythm

QRS. Conduction block in the left or right bundle branch or activation

of the ventricles from an accessory pathway produces a wide QRS complex during SVT that must be distinguished from ventricular tachycardia (VT). Mechanisms of supraventricular tachyarrhythmia can be

divided into physiologic sinus tachycardia and pathologic tachycardia

(Table 246-1).

Pathologic tachycardia can be further subclassified by mechanism

as reentrant arrhythmias dependent on AV nodal conduction (e.g.,

AVNRT), large reentry circuits within the atrial tissue alone (e.g.,

atrial flutter), or focal atrial tachycardias that can be due to automaticity or small reentry circuits. The prognosis and treatment vary

considerably depending on the mechanism and underlying heart

disease. SVT can be of brief duration, termed nonsustained, or can

be sustained such that an intervention, such as cardioversion, catheter ablation, or drug administration, is required for termination and

maintenance of sinus rhythm. Episodes that occur with sudden onset

and termination are referred to as paroxysmal. Paroxysmal supraventricular tachycardia (PSVT) refers to a family of tachycardias including

AV node reentry, AV reciprocating tachycardia using an accessory

pathway, and atrial tachycardia described in subsequent chapters

(Fig. 246-1).

CLINICAL PRESENTATION

Symptoms of supraventricular arrhythmia vary depending on the rate,

duration, associated heart disease, and comorbidities and include palpitations, chest pain, dyspnea, diminished exertional capacity, and occasionally syncope. Rarely, a supraventricular arrhythmia precipitates

cardiac arrest in patients with Wolff-Parkinson-White (WPW) syndrome or severe heart disease, such as hypertrophic cardiomyopathy.

■ INITIAL EVALUATION

The diagnosis of SVT is most often entertained when evaluating a

patient for arrhythmia-related symptoms or when evidence of ventricular preexcitation is seen on an electrocardiogram (ECG) as an

outpatient. Diagnosis of SVT requires obtaining an ECG at the time of

symptoms (Fig. 246-2). Ventricular preexcitation on the resting ECG

suggests AV reciprocating tachycardia using an accessory pathway.

When the arrhythmia is ongoing at the time of recording, the ECG

usually establishes or suggests the diagnosis. In the urgent care or

inpatient setting, treatment of SVT will often involve vagal maneuvers

or carotid sinus massage (CSM) to achieve AV block (Table 246-2).

In the appropriate patient, CSM should be used cautiously, if at all,

if there is concern for carotid atherosclerosis that may be embolized

during manipulation. If this is unsuccessful, the administration of 6 or

12 mg of adenosine to cause transient AV block is usually successful

in terminating an AV nodal–dependent SVT or diagnosing a non-AV

nodal–dependent SVT such as atrial tachycardia or atrial flutter. There

are some atrial tachycardias that are adenosine sensitive, and thus,

246 Approach to

Supraventricular

Tachyarrhythmias

William H. Sauer, Paul C. Zei

TABLE 246-1 Mechanisms of Supraventricular Tachyarrhythmia

Physiologic Sinus Tachycardia

Defining feature: normal sinus mechanism precipitated by exertion, stress,

exogenous or endogenous stimulants, concurrent illness

Pathologic Supraventricular Tachycardia (SVT)

A. Tachycardias originating from the atrium

Defining feature: tachycardia may continue despite beats that fail to conduct to

the ventricles, indicating that the atrioventricular (AV) node is not participating in

the tachycardia circuit

1. Inappropriate sinus tachycardia

Defining feature: tachycardia from the normal sinus node area that occurs

without an identifiable precipitating factor as a result of dysfunctional autonomic

regulation

2. Focal atrial tachycardia (AT)

Defining feature: regular atrial tachycardia with defined P wave; may be

sustained, nonsustained, paroxysmal, or incessant; frequent sites of origin occur

along the valve annuli of left or right atrium, pulmonary veins, coronary sinus

musculature, superior vena cava

3. Atrial flutter and macroreentrant atrial tachycardia

Defining feature: macroreentry reflected as organized atrial activity on an

electrocardiogram (ECG), commonly seen as sawtooth flutter waves at rates

typically faster than 200 beats/min

4. Atrial fibrillation

Defining feature: chaotic rapid atrial electrical activity with variable ventricular

rate; the most common sustained cardiac arrhythmia in older adults

5. Multifocal atrial tachycardia

Defining feature: multiple discrete P waves often seen in patients with pulmonary

disease during acute exacerbations of pulmonary insufficiency

B. AV nodal reentry tachycardia (AVNRT)

Defining feature: paroxysmal regular tachycardia with P waves visible at the end

of the QRS complex or not visible at all; the most common paroxysmal sustained

tachycardia in healthy young adults; more common in women

C. Tachycardias associated with accessory atrioventricular pathways

1. Orthodromic AV reciprocating tachycardia (AVRT)

Defining feature: paroxysmal sustained tachycardia similar to AV nodal reentry;

during sinus rhythm, evidence of ventricular preexcitation may be present

(Wolff-Parkinson-White syndrome) or absent (concealed accessory

pathway)

2. Preexcited tachycardia

Defining feature: wide QRS tachycardia with QRS morphology similar to

ventricular tachycardia

a. Antidromic AV reciprocating tachycardia—regular paroxysmal

tachycardia

b. Atrial fibrillation with preexcitation—irregular wide-complex or

intermittently wide-complex tachycardia, some with dangerously rapid

rates faster than 250/min

c. Atrial tachycardia or flutter with preexcitation

termination of an SVT with adenosine does not exclude this potential

diagnosis.

For transient arrhythmias, ambulatory ECG recording is warranted.

Patients will often have access to ECG recording devices, such as a

watch or smartphone-enabled electrogram recording electrode pair.

Therefore, a patient may have the ECG diagnosis before seeing a physician (Fig. 246-3).

Exercise testing is useful for assessing exercise-related symptoms and potentially evoking the arrhythmia. Additional evaluation for underlying cardiac disease and to exclude potentially

dangerous arrhythmias should be performed based on the clinical scenario. Occasionally, an invasive electrophysiology study is

warranted to provoke the arrhythmia with pacing, confirm the

mechanism, and risk stratify the patient, but most commonly, this

is performed at the time of intended catheter ablation to treat the

arrhythmia.

Approach to Supraventricular Tachyarrhythmias

1889CHAPTER 246

NARROW-COMPLEX TACHYCARDIA – OBTAIN FULL

12-LEAD ECG WITH LONG RHYTHM STRIP

Regular

atrial rate

Irregular atrial

and ventricular

rates

Atrial fibrillation VA block: more

V’s than A’s

AV block: more

A’s than V’s

1:1 AV

response

• Junctional

 tachycardia

• AVNRT

• ORT

• AT

• Rarely

 atrial flutter

• Atrial

 flutter

• Atrial

 tachycardia

• Rarely

 AVNRT with

 2:1 block

 below the

 His bundle

Multifocal atrial

tachycardia

FIGURE 246-1 Diagnostic possibilities based on the appearance of the 12-lead electrocardiogram (ECG) recorded during an episode of supraventricular tachycardia

(SVT). AT, focal atrial tachycardia; AVNRT, atrioventricular (AV) nodal reentry tachycardia; ORT, orthodromic AV reentry tachycardia.

AV nodal blockade

(Adenosine or vagal reflex maneuver)

Atrial rate continues

with AV block No effect SVT slows SVT terminated

• AVNRT

• AVRT

• Adenosine sensitive

 Focal AT

• Fascicular VT

• Inadequate dose/effect

• Sinus tachycardia

• Junctional tachycardia

• Atrial flutter

• Atrial tachycardia

FIGURE 246-2 Diagnostic effect of increasing atrioventricular (AV) node blockade with vagal maneuvers, carotid sinus massage, adenosine, verapamil, or beta blockers.

AT, focal atrial tachycardia; AVNRT, atrioventricular nodal reentry tachycardia; AVRT, atrioventricular reciprocating tachycardia; SVT, supraventricular tachycardia.

Paroxysmal SVT is most commonly encountered in patients who do

not have structural heart disease. Other supraventricular arrhythmias,

particularly atrial fibrillation, are often associated with a variety of

heart diseases. At initial evaluation, history and examination should

assess possible underlying heart disease. Any abnormal findings may

warrant further cardiac evaluation.

The most common SVT is sinus tachycardia in response to physiologic stress, such as exercise, but it can also be a manifestation

of acute illness. The first step in diagnosis of SVT is to consider

the possibility of sinus tachycardia. Therapy is then determined by

the clinical findings and probable diagnosis. If sinus tachycardia is

diagnosed, treatment of the underlying inciting cause is the primary

approach. If the arrhythmia is ongoing and is not due to sinus tachycardia, initial assessment determines whether immediate therapy is

needed to terminate the arrhythmia or slow the rate. Arrhythmias that

cause hypotension, impaired consciousness, angina, or heart failure

warrant immediate therapy, guided by the type of arrhythmia. Treatment options for specific types of SVT are discussed in more detail

in subsequent chapters and include pharmacologic and procedural

interventions.

1890 PART 6 Disorders of the Cardiovascular System

Heart Rate Over 120 — 200 BPM

Average

This ECG was not checked for AFib

because your heart rate was over 120 BPM.

If you repeatedly get this result or you’re

not feeling well, you should talk to your

doctor.

Reported Symptoms

• Rapid pounding, or fluttering heartbeat

• Chest tightness or pain

• Fainting

25 mm/s, 10 mm/mV, Lead I, 511Hz, iOS 12.1.4, watchOS 5.1.3, Watch4,2 — The waveform is similar to a Lead I ECG. For more information, see Instructions for Use.

20s 21s 22s 23s 24s 25s 26s 27s 28s 29s

10s 11s 12s 13s 14s 15s 16s 17s 18s 19s

0s 1s 2s 3s 4s 5s 6s 7s 8s 9s

FIGURE 246-3 Narrow-complex tachycardia recorded by a consumer wearable monitor (Apple watch). Afib, atrial fibrillation; ECG, electrocardiogram.

TABLE 246-2 Vagal Maneuvers

Diaphragm

Chest

muscles

Lungs

Larynx

Abdominal

cavity

Abdominal

muscles

Rectus muscles

Holding breath while bearing down to

increase intrathoracic pressure

15s

Breathing hard into a syringe against pressure

to increase intrathoracic pressure Raise legs abruptly to increase venous return

Submerge face into cold water (diver’s

reflex)

Carotid sinus

Vagus nerve

Right common

carotid artery

Sternocleidomastoid

muscle

Cardiac plexus

Carotid sinus massage

Adenosine

Adenosine

Physiologic and Nonphysiologic Sinus Tachycardia

1891CHAPTER 247

Acknowledgment

Gregory F. Michaud and William G. Stevenson contributed to this chapter in the 20th edition, and some material from that chapter has been

retained here.

■ FURTHER READING

Brugada J et al: 2019 ESC guidelines for the management of patients

with supraventricular tachycardia. The task force for the management

of patients with supraventricular tachycardia of the European Society

of Cardiology (ESC) developed in collaboration with the Association

for European Paediatric and Congenital Cardiology (AEPC). Eur

Heart J 41:655, 2020.

Callans DJ: Josephson’s Clinical Cardiac Electrophysiology: Techniques

and Interpretations, 6th ed. Philadelphia, Wolters Kluwer, 2021.

The sinus node is composed of a group of cells located in the lateral

superior aspect of the junction between the right atrium and superior

vena cava, within the superior aspect of the thick ridge of muscle

known as the crista terminalis where the posterior smooth atrial wall

derived from the sinus venosus meets the trabeculated anterior portion

of the right atrium. Patients with sinus tachycardia will often seek medical attention with the uncomfortable awareness of their heartbeat as

their chief complaint. Often, an arrhythmia is suspected because of the

similar constellation of symptoms that accompanies supraventricular

and ventricular tachycardia or atrial and ventricular ectopy. However,

a careful review of the 12-lead electrocardiogram (ECG) reveals a

characteristic P wave originating from the superior and lateral aspect

of the right atrium with a positive deflection in leads I, II, and III and

247 Physiologic and

Nonphysiologic Sinus

Tachycardia

William H. Sauer, Paul C. Zei

A B

II, III, aVF

V1

aVR

SVC

Compact

AVN

Sinus

node

IVC

Triangle of Koch

TVA

Pectinate

muscles

FO

Crista terminalis

CS Os

Eustachian

ridge

FIGURE 247-1 Right atrial anatomy pertinent to normal sinus rhythm and supraventricular tachycardia. A. Typical P-wave morphology during normal sinus rhythm based

on standard 12-lead electrocardiogram. There is a positive P wave in leads II, III, and aVF and a biphasic, initially positive P wave in aVR. B. Right atrial anatomy seen from

a right lateral perspective with lateral wall opened to view the septum. AVN, atrioventricular node; CS Os, coronary sinus ostium; FO, fossa ovalis; IVC, inferior vena cava;

TVA, tricuspid valve annulus.

a biphasic morphology in lead V1

. Sinus P waves are characterized

by a frontal plane axis directed inferiorly and leftward, with positive

P waves in leads II, III, and aVF; a negative P wave in aVR; and an initially positive biphasic P wave in V1

. Normal sinus rhythm has a range

of rates between 60 and 100 beats/min (Fig. 247-1).

PHYSIOLOGIC SINUS TACHYCARDIA

Sinus tachycardia (>100 beats/min) typically occurs in response to

sympathetic stimulation and vagal withdrawal, whereby the rate of

spontaneous depolarization of the sinus node increases and the focus

of earliest activation within the node typically shifts more leftward and

closer to the superior septal aspect of the crista terminalis, thus producing taller P waves in the inferior limb leads when compared to normal sinus rhythm. Sinus bradycardia is defined as rates <60 beats/min;

however, bradycardia can be normal during sleep and in fit individuals.

Sinus tachycardia is considered physiologic when it is an appropriate

response to exercise, stress, or illness. Sinus tachycardia can be difficult

to distinguish from focal atrial tachycardia (see below) that originates

near the sinus node. A causative factor (e.g., exertion) and a gradual

rate increase favor a diagnosis of sinus tachycardia, whereas abrupt

tachycardia onset and offset favor atrial tachycardia (Fig. 247-2).

The distinction can be difficult and occasionally requires extended

ECG monitoring or invasive electrophysiology study. Treatment for

physiologic sinus tachycardia is aimed at the underlying condition,

but frequently, no therapy is necessary. Consideration to abnormal

thyroid conditions and anemia should be given in patients with sinus

tachycardia as these represent reversible causes. In addition, structural

and functional cardiovascular abnormalities can present as sinus

tachycardia, especially pulmonary embolism, and thus must be ruled

out before considering sinus tachycardia as nonphysiologic. Finally, as

sinus rate varies widely between individuals, a relatively elevated sinus

rate (whether at rest or during exercise) without underlying cause,

particularly without symptoms, typical does not warrant treatment

(Table 247-1).

NONPHYSIOLOGIC SINUS TACHYCARDIA

Inappropriate sinus tachycardia is an uncommon condition in which

the sinus rate increases spontaneously at rest or out of proportion to

physiologic stress or exertion and is within a spectrum of ill-defined

conditions associated with autonomic dysregulation. The underlying

mechanism remains elusive, but it may be related to imbalance between

1892 PART 6 Disorders of the Cardiovascular System

sympathetic and parasympathetic inputs to the sinus node, altered

membrane automaticity of sinus node cells, or a combination of both.

Affected individuals are often women in the third or fourth decade of

life. Fatigue, dizziness, and even syncope may accompany palpitations,

which can be disabling. Additional symptoms of chest pain, headaches,

and gastrointestinal upset are common. Inappropriate sinus tachycardia must be distinguished from appropriate sinus tachycardia and from

focal atrial tachycardia arising from a region near the sinus node. The

distinction between physiologic sinus tachycardia due to an anxiety

disorder and inappropriate sinus tachycardia can be difficult. Therapy

is often ineffective or poorly tolerated. Careful titration of beta blockers

and/or calcium channel blockers may reduce symptoms. Clonidine

and serotonin reuptake inhibitors have also been used. Ivabradine,

a drug that blocks the If

 current that causes spontaneous sinus node

depolarization, is approved in the United States for use in heart failure,

but it has also been effective in the treatment of inappropriate sinus

tachycardia. Catheter ablation of the sinus node to modify and thereby

decrease the sinus rate has been performed, but long-term control of

symptoms is usually poor and can result in a permanent pacemaker

requirement due to resultant symptomatic bradycardia or chronotropic

incompetence (Fig. 247-3).

Postural orthostatic tachycardia syndrome (POTS) is characterized

by symptomatic sinus tachycardia that occurs with postural change

12 am

200

150

100

50

0

6 am 12 pm 6 pm 12 am

12 am

A

B

200

150

100

50

0

6 am 12 pm 6 pm 12 am

FIGURE 247-2 Outpatient telemetry monitor in a patient with intermittent atrial

tachycardia (A) and normal physiologic sinus tachycardia (B).

Sinus tachycardia

Identify and treat

reversible causes

(See Table 247-1)

Evaluate for POTS Treatment of POTS

• Recumbent exercise and

 conditioning regimen

• High-salt diet

• Compression stockings

• Fludrocortisone

• Midodrine

IST suspected

Beta blocker and/or

ivabradine

Consider catheter

ablation

FIGURE 247-3 Evaluation and treatment of sinus tachycardia. For the patient who

presents with sinus tachycardia, reversible causes of appropriate sinus tachycardia

must be excluded and treated as indicated. Otherwise, evaluation for a spectrum

of syndromes resulting in inappropriate sinus tachycardia should be undertaken.

Potential directed therapies are shown. IST, inappropriate sinus tachycardia; POTS,

postural orthostatic tachycardia syndrome.

TABLE 247-1 Common Causes of Sinus Tachycardia

Physiologic Causes

Emotion, physical exercise, sexual intercourse, pain, pregnancy

Pathologic Causes

Anxiety, panic attack, anemia, fever, dehydration, infection, malignancies,

hyperthyroidism, hypoglycemia, pheochromocytoma, Cushing’s disease,

diabetes mellitus with evidence of autonomic dysfunction, pulmonary embolus,

myocardial infarction, pericarditis, valve disease, decompensated heart failure,

shock, alcohol withdrawal

Drugs

Epinephrine, norepinephrine, dopamine, dobutamine, atropine, β2

-adrenergic

receptor agonists (salbutamol), methylxanthines, doxorubicin, daunorubicin, beta

blocker withdrawal, caffeine, alcohol

Illicit Drugs

Amphetamines, cocaine, lysergic acid diethylamide, psilocybin, ecstasy, cocaine

from a supine position to standing. The sinus rate increases by

30 beats/min or to >120 beats/min within 10 min of standing and in

the absence of hypotension. Symptoms are often similar to those in

patients with inappropriate sinus tachycardia. POTS is sometimes due

to autonomic dysfunction following a viral illness and may resolve

spontaneously over 3–12 months. Volume expansion with salt supplementation, oral fludrocortisone, compression stockings, and the

α-agonist midodrine, often in combination, can be helpful. Exercise

training has also been shown to improve symptoms and should be a

part of a treatment strategy to reduce symptoms. While it is sometimes

difficult to differentiate inappropriate sinus tachycardia from POTS,

recognition of these distinct clinical syndromes is critical for treatment.

Sinus node modification will be ineffective for the treatment of POTS.

Likewise, treatment strategies aimed at increasing blood pressure will

not be appropriate for inappropriate sinus tachycardia.

Acknowledgment

Gregory F. Michaud and William G. Stevenson contributed to this

chapter in the 20th edition, and some material from that chapter has

been retained here.

■ FURTHER READING

Brugada J et al: 2019 ESC guidelines for the management of patients

with supraventricular tachycardia. The task force for the management

of patients with supraventricular tachycardia of the European Society

of Cardiology (ESC) Developed in collaboration with the Association

for European Paediatric and Congenital Cardiology (AEPC). Eur

Heart J 41:655, 2020.

Mar PL, Raj SR: Postural orthostatic tachycardia syndrome: Mechanisms and new therapies. Ann Rev Med 71:235, 2020.

Olshansky B, Sullivan RM: Inappropriate sinus tachycardia. EP

Europace 21:194, 2019.

Sheldon RS et al: 2015 Heart Rhythm Society expert consensus

statement on the diagnosis and treatment of postural tachycardia

syndrome, inappropriate sinus tachycardia, and vasovagal syncope.

Heart Rhythm 12:e41, 2015.

Focal Atrial Tachycardia

1893CHAPTER 248

The underlying mechanisms of focal atrial tachycardia (AT) include

abnormal automaticity, triggered automaticity, or a small reentry

circuit in diseased atrial tissue. The term focal is used to differentiate

this form of atrial tachycardia from typical and atypical atrial flutter

but does not define a mechanism of the arrhythmia. ATs can originate

from most regions of the atria, including atrial tissue extending into a

pulmonary vein, the coronary sinus, or vena cava. It can be sustained,

nonsustained, paroxysmal, or incessant. Focal AT accounts for ~10% of

paroxysmal supraventricular tachycardia (PSVTs) in patients referred

for catheter ablation. Nonsustained focal AT is commonly observed on

ambulatory electrocardiogram (ECG) recordings, and the prevalence

increases with age. Treatment is not recommended for asymptomatic

nonsustained atrial tachycardia identified on ECG monitoring. However, frequent atrial ectopy and nonsustained AT are often precursors

to more significant arrhythmias such as atrial fibrillation and atrial

flutter. Nonsustained, frequent atrial ectopy or short bursts of AT may

be symptomatic and require therapy similar to that required for focal

AT (Fig. 248-1).

AT can occur in the absence of structural heart disease or may be

associated with any condition that causes atrial fibrosis, including prior

catheter ablation. Areas of fibrosis can act as a nidus for abnormal

automaticity from damaged cells or microreentry within zones of slow

conduction within and on the border of fibrotic areas. Sympathetic

stimulation is a promoting factor, and the emergence of AT can be a

sign of underlying illness. AT with atrioventricular (AV) block may

occur in digitalis toxicity. Symptoms from AT are highly variable but

similar to other supraventricular tachycardias (SVTs), and incessant

AT can cause tachycardia-induced cardiomyopathy.

AT typically presents with 1:1 AV conduction or with AV block

in a Wenckebach or fixed (e.g., 2:1 or 3:1) pattern. Because it is not

dependent on AV nodal conduction, AT will not terminate with AV

block, and the atrial rate will not be affected, which distinguishes

AT from most AV nodal–dependent SVTs, such as AV nodal reentry

and AV reentry using an accessory pathway (see below). A so-called

warm-up phase when the atrial activation rate increases after initiation

248 Focal Atrial Tachycardia

William H. Sauer, Paul C. Zei

or a cool-down phase when the rate slows prior to termination also

favors AT rather than AV nodal–dependent SVT, as this is a common

observation with triggered automaticity. P waves are often discrete,

with an intervening isoelectric segment, in contrast to atrial flutter and

macroreentrant AT because atrial activation from a focal source occurs

through a small portion of the tachycardia cycle (Fig. 248-2).

When 1:1 conduction to the ventricles is present, the arrhythmia can

resemble sinus tachycardia typically with a P-R interval shorter than

the R-P interval, particularly when sympathetic tone results in rapid AV

nodal conduction. It can be distinguished from sinus tachycardia by the

P-wave morphology, which usually differs from sinus P waves depending on the location of the focus. Focal AT tends to originate in areas

of complex atrial anatomy, such as the crista terminalis, valve annuli,

atrial septum, and atrial muscle extending along cardiac thoracic veins

(superior vena cava, coronary sinus, and pulmonary veins), and the

location can often be estimated by the P-wave morphology. AT from

the atrial septum will frequently have a narrower P-wave duration than

sinus rhythm. AT from the left atrium will usually have a monophasic,

positive P wave in lead V1

 and negative P waves in I and aVL, indicating an activation wavefront away from the left atrial free wall. AT that

originates from superior atrial locations, such as the superior vena cava

or superior pulmonary veins, will be positive in the inferior limb leads

II, III, and aVF, whereas AT from a more inferior location, such as the

ostium of the coronary sinus, will inscribe negative P waves in these

same leads. When the focus is in the superior aspect of the crista terminalis, close to the sinus node, however, the P wave will resemble that

of sinus tachycardia. Abrupt onset and offset then favor AT rather than

sinus tachycardia. Depending on the atrial rate, the P wave may fall

on top of the T wave, or during 2:1 conduction, it may fall coincident

with the QRS. Maneuvers that increase AV block, such as carotid sinus

massage, Valsalva maneuver, or administration of AV nodal–blocking

agents, such as adenosine, are useful to create AV block that will expose

the P wave.

Acute management of sudden-onset, sustained AT is the same as

for other forms of PSVT, but the response to pharmacologic therapy is

variable, likely depending on the mechanism (Fig. 248-3).

For AT due to reentry, administration of adenosine or vagal

maneuvers may transiently increase AV block without terminating

tachycardia. Some ATs terminate with a sufficient dose of adenosine,

consistent with triggered activity as the mechanism. Cardioversion

can be effective in some but fails in others because of immediate

recurrence, suggesting automaticity as the mechanism in these cases.

AT

AVRT

AVNRT • Av node reentry

No P w-wave visible

RP < PR

RP< PR

RP < PR

RP < PR

• AV node reentry

• AV reentry using an

accessory pathway

• Focal atrial tachycardia

• AV reentry using an

accessory pathway

• AV node reentry

uncommon form

FIGURE 248-1 Common mechanisms underlying paroxysmal supraventricular tachycardia along with typical R-P relationships. A. Schematic showing a four-chamber

view of the heart with atrioventricular (AV) node and specialized conduction tissue (His-Purkinje) in yellow. Atrial tachycardia (AT; red circuit) is confined completely to atrial

tissue. Atrioventricular nodal reentry tachycardia (AVNRT; green circuit) uses AV nodal and perinodal atrial tissue. Atrioventricular reentry tachycardia (AVRT; blue circuit)

uses atrial and ventricular tissue, accessory pathway between the ventricle and atrium, AV node, and His-Purkinje tissue as part of the reentry circuit. B. Typical relation of

the P wave to QRS, commonly described as the R-P to P-R relationship, for the different tachycardia mechanisms.

1894 PART 6 Disorders of the Cardiovascular System

Adenosine Cardioversion

Hemodynamic

instability

No Yes

Focal atrial tachycardia

Non-DHP CCB

and/or beta blocker

Recurrent

or incessant

Ineffective

Ineffective

Ineffective

Recurrent

or incessant

Antiarrhythmic therapy

(see Table 243-2)

Catheter

ablation

FIGURE 248-3 Clinical approach and treatment algorithm for management of

focal atrial tachycardia. CCB, calcium channel blocker; DHP, dihydropyridine.

(Adapted from J Brugada et al: 2019 ESC Guidelines for the management

of patients with supraventricular tachycardia The Task Force for the

management of patients with supraventricular tachycardia of the European

Society of Cardiology (ESC) [published correction appears in Eur Heart J. 2020

Nov 21;41(44):4258]. Eur Heart J 41:655, 2020.)

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

VI

V5

III

I aVR

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

VI

V5

III

aVR

FIGURE 248-2 Focal atrial tachycardia. In the right panel, a surface 12-lead electrocardiogram shows focal intermittent atrial tachycardia. Note the discrete P waves, with

isoelectric segments between, as well as the sinus rhythm. The left panel shows an electroanatomic map of the same focal atrial tachycardia originating from the anterior

interatrial septum, as viewed in an anterior-posterior (AP) view of the left atrium obtained during electrophysiology study and ablation. The colors represent the timing of

local electrical activation during each tachycardia atrial activation, showing a focal early (red) site. Additional markers of white “flecks” represent conduction direction,

demonstrating activation of the atrium dispersing from this focal site. Of note, the pink and red dots represent ablation lesions, in this case, for pulmonary vein isolation.

(Adapted from J Brugada et al: 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with

supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J 41:655, 2020.)

In this chapter, sustained supraventricular tachycardias (SVTs) dependent on the atrioventricular (AV) node are discussed. These include

AV nodal reentry tachycardia (AVNRT), junctional tachycardia, AV

reciprocating tachycardia (AVRT) utilizing an accessory pathway, and

a group of additional various SVTs that involve an accessory pathway,

termed preexcited tachycardias. The term SVT encompasses a broad

group of tachyarrhythmias based on anatomic origin and technically

includes sinus tachycardia, atrial tachycardia (AT), atrial flutter, and

atrial fibrillation; however, for the purposes of describing an organized

approach to diagnosis and treatment of SVT, a separate discussion for

these non-AV nodal–dependent SVTs are discussed elsewhere.

249 Paroxysmal

Supraventricular

Tachycardias

William H. Sauer, Paul C. Zei

Beta blockers and calcium channel blockers may slow the ventricular rate

by increasing AV block, which can improve tolerance of the arrhythmias,

but large doses are sometimes required. Potential precipitating factors

and intercurrent illness should be sought and corrected. Underlying

heart disease should be considered and excluded.

For patients with recurrent episodes, beta blockers, calcium channel

blockers such as diltiazem or verapamil, and antiarrhythmic drugs

such as flecainide, propafenone, disopyramide, sotalol, and amiodarone can be effective, but potential toxicities and adverse effects often

warrant avoidance of long-term use.

Catheter ablation targeting the AT focus is effective in >80% of

patients and is recommended for recurrent symptomatic AT when

drugs fail or are not desired or for incessant AT causing tachycardiainduced cardiomyopathy. Although AT is often a precursor to atrial

fibrillation or atrial flutter, the associated risk for stroke and hence

indications for long-term anticoagulation are unclear but not considered equivalent.

Acknowledgment

Gregory F. Michaud and William G. Stevenson contributed to this chapter in the 20th edition and some material from that chapter has been

retained here.

■ FURTHER READING

Brugada J et al: 2019 ESC Guidelines for the management of patients

with supraventricular tachycardia. The Task Force for the Management

of Patients with Supraventricular Tachycardia of the European

Society of Cardiology (ESC) developed in collaboration with the

Association for European Paediatric and Congenital Cardiology

(AEPC). Eur Heart J 41:655, 2020.

Callans DJ: Josephson’s Clinical Cardiac Electrophysiology: Techniques

and Interpretations, 6th ed. Philadelphia, Wolters Kluwer, 2021.