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Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier
Chapter 63 – CARDIAC ARRHYTHMIAS WITH SUPRAVENTRICULAR ORIGIN
Masood Akhtar
Definition and Pathobiology
Both of the atria and corresponding ventricles are electrically insulated from each other by
fibrous tissue that is the anatomic atrioventricular (AV) junction. The fibrous structures in the AV
junction are the annuli of the mitral and tricuspid valves and the fibrous portion of the
interventricular septum. In the absence of an electrical bridge, the atrial impulses cannot cross
this fibrous gap. Normally, the AV node and the connected His-Purkinje system (HPS) provide
the only electrical conduit. Some individuals, however, have additional electrical bridges, which
bypass the AV node–HPS to connect the atria directly with ventricles or fascicles. These
pathways, often referred to as accessory pathways, include AV connections (Kent bundle),
which form the anatomic basis for Wolff-Parkinson-White (WPW) syndrome, and atriofascicular
fibers (previously called Mahaim fibers).
Any arrhythmia that arises above the bifurcation of the His bundle into the right and left bundle
branches or activates the ventricles through an accessory pathway is classified as
supraventricular. The resultant QRS complex morphology either can be normal or may be wide
owing to bundle branch or fascicular block (aberrant conduction) or conduction over an
accessory pathway (anomalous conduction or preexcitation). Supraventricular cardiac
arrhythmias can be categorized broadly into tachyarrhythmias or bradyarrhythmias.
TACHYARRHYTHMIAS
Definition
Supraventricular tachyarrhythmias can occur either as single or consecutive premature

complexes or in the form of nonsustained or sustained tachycardias. The most frequent
definition of nonsustained tachycardias is an arrhythmia with a rate of more than 100 beats per
minute lasting 3 beats or more but less than 30 seconds. Sustained tachycardia is a prolonged
episode of tachycardia lasting at least 30 seconds or terminated earlier with an intervention,
such as intravenous medication, overdrive pacing, or direct current electrical cardioversion
because of the urgency of the situation.
Premature Atrial Complexes
Premature atrial complexes (PACs) can arise from any part of the right or left atrium or any
adjacent tissue where a sleeve of atrial muscle extends, such as the pulmonary veins. The P
wave morphology depends on the origin but differs from sinus rhythm unless PACs arise near
the upper right atrial junction with the superior vena cava, that is, close to the location of sinus
node. The P wave always precedes the QRS complex (Fig. 63-1A); if it encounters the absolute
refractory period of the AV node or the HPS, the P wave is blocked and is not followed by a
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QRS complex. A blocked PAC may be confused with second-degree AV block unless its
prematurity is recognized or with sinus node dysfunction (SND) if it is inconspicuous. Altered
appearance of the ST-T segment is often a clue to the presence of a P wave. When a
premature QRS complex has the morphology of the underlying sinus rhythm but is not
preceded by a P wave, it is labeled AV junctional (see Fig. 63-1B). When two or more
morphologically distinct P waves result in a rate less than 100 beats per minute, the rhythm is
termed wandering atrial pacemaker.
FIGURE 63-1 Isolated premature complexes. A, Three premature atrial complexes (arrows). The first one is blocked,
whereas the remaining two conduct to the ventricles with QRS morphology different from that of sinus complexes owing to
encroachment of premature impulses on the refractory period of the His-Purkinje system (aberrant conduction). B, Premature
junctional complex (fifth complex). Note the similarity of the QRS complex between the sinus and premature beat that is not
preceded by a P wave. The next sinus P wave (arrow), which is superimposed on the T wave of the premature beat, occurs on
time and conducts to the ventricles. Electrocardiographic leads are labeled.
(Modified from Akhtar M: Examination of the heart: Part V. The electrocardiogram, 1990. With permission from the American
Heart Association, Dallas, TX.)
Premature complexes from the atria or AV junction usually lead to the same intraventricular
conduction pattern seen during sinus complexes; that is, if the sinus rhythm shows a normal
QRS complex or bundle branch block pattern, the same configuration would be expected during
the premature complexes (see Fig. 63-1B). If the premature complexes are relatively early (i.e.,
closely coupled), however, they can encroach on the refractory period of the right or left bundle
branches, resulting in aberrant conduction and producing a right or left bundle branch or
fascicular block pattern (see Fig. 63-1A) despite normal intraventricular conduction during sinus
rhythm. Closely coupled PACs also frequently initiate sustained or nonsustained
supraventricular tachycardias.
Sustained Supraventricular Tachycardias
Supraventricular tachycardias can be categorized broadly into atrial and AV junctional (Table
63-1). Atrial tachycardias are independent of AV nodal conduction, so that effective vagal
maneuvers (e.g., carotid sinus massage, Valsalva) or medications that slow AV nodal
conduction cause AV block, but the atrial process continues (Fig. 63-2A). Conversely, most AV
junctional tachycardias require propagation through the AV node to continue, and AV junctional
tachycardias generally terminate if vagal maneuvers induce AV nodal block (see Fig. 63-2B).
TABLE 63-1 -- SUPRAVENTRICULAR TACHYCARDIAS

R-R Regularity P Wave Morphology
Atrial tachycardias
Sinus tachycardia Regular Positive in II, III, aVF
Sinus node re-entry Regular Positive in II, III, aVF
Atrial tachycardia, unifocal Regular P different from sinus
Atrial tachycardia, multifocal Irregular ≥3 different P wave morphologies
Atrial flutter, common, Regular, irregular if Sawtooth flutter waves; regular
counterclockwise variable AV block waveform; negative in II, III, aVF
Atrial flutter, uncommon, Regular, irregular if Upright flutter waves; positive waveform
clockwise variable AV block II, III, aVF
Atrial fibrillation Irregularly irregular Irregular fibrillation waves
AV junctional tachycardias
AV re-entry (using
accessory pathways)
Orthodromic Regular Retrograde P in ST-T wave
Antidromic Regular preexcited Retrograde P, short RP
Slow conducting Regular Retrograde P at end of T wave or later
(long RP)
Atriofascicular Regular preexcited Retrograde P, short RP
(antidromic)
AV nodal re-entry
Common (slow-fast) Regular Retrograde P obscured by QRS or alters
the end of QRS (short RP)
Uncommon (fast-slow) Regular Retrograde P at end of T wave or later
(long RP)
Others (slow-slow) Regular PR-RP approximately equal
Nonparoxysmal junctional Regular, slow rate AV dissociation
tachycardia [*]
Automatic junctional Regular AV dissociation
tachycardia [*]
* Site of origin usually infranodal. AV = atrioventricular.
FIGURE 63-2 P-QRS relationship in supraventricular tachycardia. Sinus rhythm (A), usual type of sinus tachycardia (B),
and unifocal atrial tachycardia (C) are shown. Note the positive P wave and normal PR interval during sinus tachycardia. Atrial
tachycardia (C) originates in the low atrium (negative P wave) and is accompanied by a variable degree of atrioventricular (AV)
block. Among the AV junctional tachycardias, the P wave follows the QRS and is in the ST segment during AV re-entry (D) and
buried in the QRS complex during common AV nodal re-entry (E). Nonparoxysmal junctional tachycardia in which the atria and
ventricles are stimulated independently is shown (F). Resultant AV dissociation occurs because the junctional rate accelerates
and competes with the sinus mechanism. Note the gradual march of P waves in and out of the QRS. Electrocardiogram lead II
in all panels.
Atrial Tachycardias
Sinus Tachycardia
Sinus tachycardia is usually due to an enhancement of normal automaticity seen in the settings
of increased adrenergic drive. Because sympathetic stimulation and vagal withdrawal also
enhance AV nodal conduction, the PR interval is not prolonged despite acceleration of the sinus
rate. The P wave configuration is the same as with sinus rhythm—upright in leads II, III, and
aVF (see Fig. 63-2A and B) and biphasic in V1—because of the normal sequence with which
the sinus node depolarizes the two atria. The atrial rate during sinus tachycardia seldom
exceeds 200 beats per minute and is generally less than 150 beats per minute.
Sinus Node Re-Entry
The P wave morphology is similar to sinus rhythm, but the underlying mechanism is re-entry in
the region of the sinus node. In contrast to the physiologic form of sinus tachycardia, which has
a gradual onset and termination, sinus node re-entry starts and ends abruptly. As with many
other atrial re-entrant tachycardias, sinus node re-entry is generally triggered by a PAC.
Sudden acceleration of the atrial rate prolongs the PR interval or may lead to AV nodal block
owing to the expected physiologic delay in AV nodal conduction unless subsequent sympathetic
stimulation facilitates AV nodal conduction. The atrial rates range between 150 and 250 beats
per minute. Depending on the state of AV conduction, 1:1 AV conduction or a variable degree
of AV block may be noted.
Atrial Tachycardia
Any tachycardia arising above the AV junction that has a P wave configuration different from
sinus rhythm is called atrial tachycardia (see Fig. 63-2C). In general, impulses arising in the
superior portion of the right or left atrium produce a positive P wave in the inferior leads (i.e.,
leads II, III, and aVF), whereas impulses arising in the lower or inferior portions result in
negative P waves in the same leads. Atrial tachycardias can result from enhanced normal
automaticity, abnormal automaticity, triggered activity, and re-entry (Chapter 60). The re-entrant
forms can be reproduced easily in the electrophysiology laboratory with electrical stimulation of
the atria (Chapter 61). When the P wave configuration is uniform from beat to beat, the
tachycardia is unifocal; the term multifocal atrial tachycardia implies several different P wave
morphologies. Atrial rates range between 100 and 250 beats per minute, and the ventricular
response depends on the status of AV conduction; a 1:1 ratio of P wave to QRS complex is
common with rates less than 200 beats per minute, whereas at higher rates various degrees of
block (e.g., 3:2, 2:1, 3:1) are common (see Fig. 63-2C). Atrial rates and AV conduction can be
altered markedly by cardioactive drugs, particularly antiarrhythmic agents.
Atrial Flutter
Atrial flutter causes regular atrial rates ranging from 250 to 350 beats per minute (300 being the
most common). Common atrial flutter, with a “sawtooth” appearance in leads II, III, and aVF,
has a fairly uniform route of impulse propagation localized to the right atrium. The re-entrant
impulse travels over the anterolateral right atrium, through a narrow isthmus in the
posteroseptal area, then along the atrial septum toward the superior portion of the right atrium
(counterclockwise). Incidental left atrial activation produces a negative sawtooth flutter wave in
the inferior leads. A reverse of this direction in the circuit could cause a positive flutter wave in
the same leads (uncommon or clockwise); both clockwise and counterclockwise atrial flutters
are also referred to as isthmus dependent. Flutter waves with other configurations may have
different origins, including the left atrium. At atrial rates of 300 beats per minute, the ventricular
response is usually 2:1 (Fig. 63-3A) or 4:1, representing ventricular rates of 150 and 75 beats
per minute, respectively. A 3:1 AV ratio is uncommon and fairly well tolerated. A 1:1 AV
response is rare and can cause serious hemodynamic consequences.
FIGURE 63-3 Atrial flutter and atrial fibrillation. A, Regular narrow QRS tachycardia with ventricular rate of 150 beats per
minute, most commonly seen in atrial flutter with 2:1 atrioventricular (AV) block. B, With a higher degree of AV block, the flutter
waves can be seen more clearly, and in this case, the atrial flutter converted briefly to atrial fibrillation (at the arrow), then to
sinus rhythm. C and D, Atrial fibrillation. The atrial activity is difficult to identify in C, but it is clear in D; in both tracings, the R-R
intervals are irregularly irregular. Two consecutive QRS complexes related to aberrant conduction (right bundle branch block)
are noted in D.
Atrial Fibrillation
Atrial fibrillation (AF) is the most common sustained arrhythmia in adults. More than 2 million
individuals in the United States have AF, with at least 160,000 new cases diagnosed every
year. The incidence of AF increases with advancing age, affecting more than 6% of the
population older than 75. A rapidly firing focus in one or more of the pulmonary veins is the
usual trigger, with subsequent disorganized and asymmetrical conduction through the atria
resulting in multiple wavelets of re-entry to sustain the AF. During AF, the atria have
disorganized, rapid, irregular electrical activity exceeding 400 beats per minute (see Fig. 63-3B
and 3C). The ventricular response is also irregular and variable (irregularly irregular). The atria
do not contract effectively so that intra-atrial clot formation is promoted. With subsequent
resumption of atrial contraction, embolism can occur with devastating consequences. On the
surface electrocardiogram (ECG), the AF waves may be coarse, fine, or difficult to discern, but
the irregularity of the RR wave makes the diagnosis of AF relatively easy. Aberrant conduction
may be noted if the impulses reach the bundle branches during their refractory period (see Fig.
63-3D). In the absence of accessory pathways, the average ventricular response by the AV
node–HPS is seldom more than 200 beats per minute and is generally less than 150 beats per
minute. With a rapidly conducting accessory pathway, ventricular rates can exceed 300 beats
per minute, however, and precipitate ventricular fibrillation.
Atrioventricular Junctional Tachycardia
Most AV junctional tachycardias (see Table 63-1) requiring long-term management are re-
entrant. AV re-entry in the WPW syndrome is the classic example and is usually (>90%)
initiated by atrial or ventricular premature complexes, or both.
Wolff-Parkinson-White Syndrome and Associated Tachycardias
A combination of a short PR interval and initial slurring of the QRS (Fig. 63-4A) is termed
ventricular preexcitation, which in association with a history of tachycardia constitutes the WPW
syndrome. Normally, the sinus impulse must travel through the AV node–HPS to reach the
ventricles, resulting in a PR interval of 120 to 200 msec. When an accessory pathway (often
called the Kent bundle) directly connects the atrium with the ventricle, it bypasses the AV nodal
conduction delay and the impulse reaches the ventricles sooner than expected, hence the term
preexcitation (Chapter 60). The length of the PR interval is a function of proximity of the
accessory pathway to the origin of impulse and conduction time through it. When location or
relatively slow conduction delays the accessory impulse, ventricular depolarization may occur
through the normal pathway. In a typical case of WPW, however, the impulse reaches the
ventricle first through the accessory pathway and starts the QRS earlier, resulting in a shorter
PR interval.
FIGURE 63-4 Wolff-Parkinson-White syndrome. A, Ventricular preexcitation (short PR and delta wave) owing to earlier
ventricular activation through the accessory pathway. B, Narrow QRS tachycardia with anterograde conduction over the
atrioventricular node–His-Purkinje system and retrograde propagation through the accessory pathway (orthodromic
tachycardia). C, The reversal of this re-entrant circuit produces antidromic tachycardia with regular and preexcited complexes.
D, During atrial fibrillation, preferential conduction over the accessory pathway produces rapid irregular preexcited complexes.
Because the initial QRS activation is due to muscle-to-muscle conduction, as opposed to

Purkinje-to-muscle activation during normal QRS, the beginning of the QRS is slurred and
produces a so-called delta wave. Soon after, ventricular activation also starts through the
normal pathway and is spread more rapidly through the ventricular myocardium, resulting in a
fusion QRS activation with a rapid inscription after the delta wave. If the atrial or sinus impulse
never reaches the ventricle through the accessory pathway because of either delayed arrival at
or lack of anterograde conduction over the accessory pathway, the term concealed WPW
syndrome is used because retrograde conduction through the accessory pathway may be intact
and able to cause orthodromic tachycardia. The most common accessory pathway (>50%) is in
the left ventricle free wall, that is, left atrium–to–left ventricle connection. Posteroseptal
pathways (connecting the right atrium with the left ventricle) are the next most common (30%).
Right free wall and anteroseptal accessory pathways, both of which are right atrium–to–right
ventricle connections, account for the remaining pathways.
The most common sustained arrhythmia in patients with WPW syndrome is orthodromic AV re-
entry (see Fig. 63-2D and 4B), in which the impulse propagates to the ventricles by means of
the normal pathway and in retrograde fashion to the atria through the accessory pathway; there
is no evidence of ventricular preexcitation during the tachycardia. In rare instances, the circuit of
re-entry may be reversed (antidromic) so that the impulse reaches the ventricle through the
accessory pathway and in retrograde conducts to the atria through the normal pathway and
produces a preexcited QRS complex (see Fig. 63-4C). The second most common arrhythmia
and frequently the most serious is AF (see Fig. 63-4D), which is experienced by 40% of patients
with WPW syndrome. If the accessory pathway conducts rapidly during AF, a relatively fast
ventricular rate may occur and cause severe hypotension or syncope, or both, and even
precipitate ventricular fibrillation. Other accessory pathways implicated in clinical tachycardias
are the atriofascicular fibers (previously referred to as Mahaim fibers) and slowly conducting
retrograde pathways.
Atrioventricular Nodal Re-entry
In the absence of ventricular preexcitation, the most common AV junctional tachycardia is AV

nodal re-entry (AVNR). The entire re-entry circuit is localized to the region of the AV node and
results from differences of conduction and refractory periods in various portions of the AV node.
Faster conducting fibers (fast pathway) are situated more anteriorly and have longer refractory
periods, whereas slower conducting fibers are posterior and have a shorter refractory period. In
the common type of AVNR, anterograde conduction is over the slow pathway and retrograde
conduction is through the fast pathway such that the conduction times of the impulse
anterograde to the ventricles and retrograde to the atria are similar (see Fig. 63-2E), resulting in
near-simultaneous P and QRS complexes. The retrograde P wave either is obscured by the
QRS complex or alters the appearance of the terminal portion of the QRS and may be
recognized in the early part of the ST segment. This type of AVNR is also referred to as slow-
fast AVN re-entry. Less frequently, the direction of conduction through the re-entry circuit is
reversed, with anterograde conduction to the ventricle over the fast pathway and retrograde
conduction to the atria through the slow pathway; the result is a shorter PR interval (fast-slow).
If the P wave follows the T wave, its retrograde morphology (i.e., negative in leads II, III, and
aVF) is clearly recognizable. Sustained AVNR and AV re-entry together account for more than
75% of cases, frequently but incorrectly labeled as paroxysmal atrial tachycardia.
Nonparoxysmal Junctional Tachycardia
Nonparoxysmal junctional tachycardia arises within the region of the His bundle and activates
the ventricles with a QRS morphology similar to that of sinus beats (see Fig. 63-2F). Retrograde
conduction through the AV node may or may not take place. If there is retrograde block, sinus
rhythm remains uninterrupted, and the sinus P wave also blocks when the AV node is refractory
because of retrograde AV nodal penetration of the junctional impulse; AV dissociation may
Chapter 63CARDIAC ARRHYTHMIAS WITH SUPRAVENTRICULAR ORIGIN ... Página 10 de 22
result. A 1:1 P wave–QRS complex relationship may also occur in some situations, and if the P
wave is negative, junctional origin is suggested. Ventricular rates seldom exceed 150 beats per
minute, and when the rate is less than 100 beats per minute, the term accelerated junctional
rhythm is applied. The underlying mechanism is enhanced normal automaticity.
Automatic Junctional Tachycardia
The main difference between automatic junctional tachycardia and nonparoxysmal junctional
tachycardia on the surface ECG is the rate. In the automatic variety, rates are faster (range,
130 to 200 beats per minute). This arrhythmia can be episodic or persistent. Because the rates
are fairly comparable to those of paroxysmal AV junctional re-entrant tachycardia and the QRS
complex morphology is similar to that of sinus beats, the presence of AV dissociation is the
main distinction from re-entrant arrhythmias on the ECG. The underlying cause is abnormal
automaticity in the AV junction.
Clinical Manifestations
The usual type of sinus tachycardia is caused by increased metabolic demands from high
adrenergic states, such as fever, physical exertion, hypovolemia, heart failure (Chapter 57),
sympathomimetic or parasympatholytic medications, thyrotoxicosis (Chapter 244), and
pheochromocytoma (Chapter 246). Sinus tachycardia is an appropriate response to the need
for an increase in cardiac output, and the accelerated rate is seldom the major symptom. All
other supraventricular tachycardias represent abnormalities of rhythm and commonly produce
tachycardia-related symptoms, including palpitation, racing of the heart, dizziness, shortness of
breath, chest discomfort, presyncope, and sometimes frank syncope. Incessant
supraventricular tachycardia and uncontrolled ventricular rates in AF can cause tachycardia-
related cardiomyopathy, which is reversible with control of these arrhythmias.
Atrial dilation, fibrosis, and acute or chronic inflammatory states involving atrial myocardium or
pericardium may cause atrial tachycardias. Multifocal atrial tachycardia is relatively frequent in
the presence of chronic pulmonary disease. AF is often associated with aging, hypertension,
valvular and pulmonary diseases, acute and chronic coronary disease, hyperadrenergic states,
and metabolic abnormalities such as diabetes and thyrotoxicosis. AF may also be noted in the
absence of any detectable cardiac pathology, in which case it is termed lone AF. The risk of
thromboembolism in AF increases with age, diabetes mellitus, hypertension, previous embolic
episodes, valvular disease, and heart failure. The lowest incidence (<1% annually) is in patients
younger than 65 years with lone AF.
Re-entrant tachycardias have an abrupt onset and an abrupt ending, particularly when
terminated with vagal maneuvers or intravenous medications. Although a functioning accessory
pathway is a congenital abnormality, its clinical manifestation can occur at any age. If no ECG
is obtained, asymptomatic ventricular preexcitation can go undetected for many years. When
discovered, ventricular preexcitation can mimic inferior or anteroseptal myocardial infarction,
right ventricular hypertrophy, and right and left bundle branch block. WPW syndrome is not
clearly associated with mitral valve prolapse or hypertrophic cardiomyopathy, but single and
multiple right-sided accessory pathways are more common with Ebstein's anomaly.
Nonparoxysmal AV junctional tachycardia is seen frequently with high adrenergic drive, that is,
after myocardial infarction or cardiac surgery, with sympathomimetic and parasympatholytic
agents, or with digitalis toxicity. Automatic junctional tachycardia is not known to be associated
with any particular cardiovascular pathology.
Treatment
See Tables 63-2 and 63-3. See also Chapter 65.
TABLE 63-2 -- SELECTION OF MEDICATIONS FOR SPECIFIC SUPRAVENTRICULAR

ARRHYTHMIAS
Acute Intravenous Long-Term Oral Long-Term
Arrhythmia Management Therapy [*] Anticoagulation
Atrial fibrillation Verapamil, diltiazem, No organic cardiac Not necessary
metoprolol, or digoxin disease—classes IA IC,
for rate control class III, amiodarone
Ibutilide for Heart failure— Yes
cardioversion amiodarone or dofetilide
Yes
Hypertension—sotalol
or class IC
Atrial fibrillation with rapid Ibutilide or Amiodarone, sotalol, or No
rate owing to Wolff- procainamide; avoid class IA or IC
Parkinson-White verapamil or digoxin
syndrome
Atrial flutter Verapamil, diltiazem, Amiodarone, sotalol, Yes
metoprolol, esmolol, class IA or IC
or digoxin
Paroxysmal Adenosine, β-Blockers, calcium- No
supraventricular verapamil, channel blockers, class
tachycardia propranolol, esmolol, IA or IC, or sotalol
or metoprolol
Adapted in part from Scheinman MM, Kaushik V: Recognition and management of patients with
tachyarrhythmias. In Braunwald E, Goldman L (eds): Primary Care Cardiology, 2nd ed.
Philadelphia, WB Saunders, 2003, pp 503–528.
* Class IA = procainamide, quinidine, disopyramide; class IC = flecainide, propafenone; class III = sotalol, dofetilide.
TABLE 63-3 -- DRUGS AND DOSES USED TO TREAT SUPRAVENTRICULAR

TACHYCARDIAS
Intravenous Intravenous
Drug Bolus Infusion Oral Dose
Digoxin 0.5–1 mg 0.125–0.5 mg/day
Adenosine 6–12 mg
β-Blockers
Esmolol 5 µg/kg/min 3 µg/kg/min
Propranolol 1–3 mg 10–40 mg tid
Metoprolol 5 mg (can 25–200 mg/day (or 12.5–100 mg bid)
repeat × 2)
Calcium-channel blockers
Verapamil 5–15 mg 120–480 mg/day (3–4 times per day in
divided doses or use long-acting form)
Diltiazem 15–25 mg 15 mg/kg 120–360 mg/day (2–3 times per day in
divided doses or use long-acting form)
Class IA
Procainamide 10–15 mg/kg 5 mg/kg 750–1500 mg qid
Quinidine 300–600 mg qid
Disopyramide 100–200 mg tid
Class IC
Flecainide 50–200 mg bid
Propafenone 150–300 mg tid
Class III
Ibutilide 1–2 mg
Sotalol 80–160 mg bid
Dofetilide 125–500 mg bid
Amiodarone 2–3 mg/kg 0.5–1 mg/min 600–1200 mg/day for 7- to 10-day loading
dose, then 100–400 mg/day, aiming for 100–
200 mg/day maintenance dose by 3 months
Acute Therapy
Isolated premature beats seldom pose significant risk, do not cause severe arrhythmic
symptoms, and do not warrant aggressive therapy. Conversely, sustained or prolonged
repeated episodes of nonsustained supraventricular tachycardias generally require effective
therapy. Whenever rapid control of supraventricular tachycardia is desired (e.g., in patients
with myocardial ischemia or hypotension), cardioversion is the best solution (Chapter 65).
Atrial tachycardias, including atrial flutter or AF, may also convert spontaneously or convert
after treatment of an underlying cause, such as hypoxia or heart failure, or after cessation of
precipitating medications.
An acute episode of junctional tachycardia from either AVNR or AV re-entry can usually be
terminated with vagal maneuvers, such as carotid massage, which produce sinus slowing
and AV nodal block. In most atrial tachycardias, adenosine (see Table 63-3) or vagal
stimulation, or both, produce enough AV block to unmask the atrial origin of the tachycardia.
However, some atrial tachycardias, particularly those arising near the sinus node, may also
terminate after administration of adenosine. Intravenous β-blockers and calcium-channel
blockers (see Table 63-3) can be used for the same purpose. For sustained control of the
ventricular rate during atrial tachycardia, intravenous esmolol and diltiazem are effective.
For acute AF without hypotension, rate control is crucial and can be accomplished with
esmolol, metoprolol, verapamil, or diltiazem (see Table 63-3); digoxin is usually a third-line
agent (Fig. 63-5). All patients with new-onset AF should receive anticoagulation acutely with
heparin (Chapter 35). If the patient is seen within 8 hours of the onset of AF,
transesophageal echocardiography should be performed (Chapter 53); if no clot is detected
in the left atrium, it is safe to proceed to cardioversion followed by warfarin anticoagulation
for 4 weeks. If transesophageal echocardiography detects clot, however, the patient should
receive at least 3 weeks of oral anticoagulation before elective cardioversion. A variety of
medications can be used to sustain sinus rhythm in patients with AF. Amiodarone (see Table
63-3) is the most effective but should be used selectively because of its potential side
effects. If ventricular response during AF is through a rapidly conducting accessory pathway,
intravenous digitalis and calcium-channel blockers are contraindicated, and procainamide is
a better choice.
Long-Term Management
For symptomatic patients with sustained AV junctional re-entry, control sometimes can be
achieved with digitalis, β-blockers, and calcium-channel blockers or with class I and class III
drugs (see Table 63-3). In patients with atrial tachycardia or atrial flutter, ventricular rate
control is possible through AV nodal block with digitalis, β-blockers, and calcium-channel
blockers. Radio frequency ablation, which is curative, is now the preferred choice for most
symptomatic sustained regular re-entrant supraventricular tachycardias, including atrial
tachycardia and atrial flutter (Chapter 65).
For prevention of recurrent AF, oral amiodarone is significantly more effective than
propafenone or sotalol, which are usually the recommended alternatives (see Table 63-2).
For most patients with AF, however, control of the ventricular rate, usually to less than about
80 beats per minute at rest and no more than 100 to 110 per minute with exercise (typically
with diltiazem, verapamil, metoprolol, or digoxin), combined with chronic warfarin
anticoagulation is as good as attempts to restore and maintain sinus rhythm with medication
or cardioversion, or both, in terms of longevity and quality of life. [1–3] In occasional patients
with chronic AF, however, the loss of the atrial contraction may be sufficient to exacerbate
symptoms of heart failure or low cardiac output despite rate control and medications for
heart failure. In these situations, radio frequency ablation of the AF focus, usually in a
pulmonary vein, can be curative. [4] Whether this approach or other catheter-based
treatments will become first-line treatment is still unproved
In patients with recurrent paroxysmal AF, another alternative is oral, out-of-hospital, self-
administration (“pill in the pocket”) of either propafenone (600 mg for patients who weigh >70
kg, 450 mg otherwise) or flecainide (300 mg for patients who weigh >70 kg, 200 mg
otherwise) after first demonstrating the safety and efficacy of either drug in the hospital
setting. In this subgroup of patients, outpatient self-treatment is 84% successful and can
reduce emergency department visits and hospitalizations.
Long-term anticoagulation therapy with warfarin is generally recommended in all patients

who are older than 65 years, who have persistent or paroxysmal AF, and who have no
contraindications to anticoagulation. [5] Warfarin alone is superior to the combination of
clopidogrel and aspirin. [6] The international normalized ratio (INR) goal is 2.0 to 3.0 unless
mitral stenosis is present, in which case the target is an INR of 2.5 to 3.5. Aspirin may be
better than no treatment for patients who cannot tolerate warfarin (Chapter 35). The addition
of aspirin to moderate-intensity warfarin in anticoagulation (INR 2.0 to 3.0) can decrease
vascular events [5,7] and is recommended in high-risk patients. Because atrial flutter also
carries a 3% per year risk of thromboembolism, patients with atrial flutter should also receive
long-term anticoagulation.
FIGURE 63-5 Management of recent-onset atrial fibrillation. IV, intravenous; LV, left ventricular, TEE, transesophageal
echocardiography.
(From Scheinman MM, Kaushik V: Recognition and management of patients with tachyarrhythmias. In Braunwald E, Goldman L
[eds]: Primary Cardiology, 2nd ed. Philadelphia, WB Saunders, 2003, p 510. Reprinted, by permission, from Falk RH: Atrial
fibrillation. N Engl J Med 2001;344:1067-1078.)
BRADYARRHYTHMIAS
Bradyarrhythmias (Table 63-4) can be classified broadly into SND and AV blocks.
TABLE 63-4 -- BRADYCARDIAS

SINUS NODE DYSFUNCTION
Sinus bradycardia <45/min

Sinoatrial exit block
First degree
Second degree
Third degree
Sinus arrest
Bradycardia-tachycardia syndrome
ATRIOVENTRICULAR BLOCK
First degree
Second degree
Mobitz type I (Wenckebach
phenomenon)
Mobitz type II
Higher degree (e.g., 2:1, 3:1)
Third degree
Atrioventricular node
His-Purkinje system
Sinus Node Dysfunction
Among the various pacemaker cells distributed throughout the cardiac conduction system, the
sinus node has the highest rate of automaticity, and it functions as the dominant pacemaker
(Chapter 60). The usual sinus rate varies between 60 and 100 beats per minute, determined by
physiologic need and modulated through the autonomic nervous system. SND has several
different manifestations, including sinus bradycardia, sinoatrial (SA) exit block, sinus arrest, and
bradycardia-tachycardia syndrome.
Sinus Bradycardia
Rates less than 60 beats per minute are usually described as bradycardia (Fig. 63-6A). In
healthy persons, rates of 50 beats per minute are not unusual, however, and rates of 30 beats
per minute may be recorded during sleep. Sinus bradycardia of clinical significance is usually
defined as persistent rates less than 45 beats per minute while awake. SND may also be
manifested by the failure to accelerate the sinus rate (lack of chronotropic response) in
situations such as exercise, heart failure, fever, sympathomimetic drugs, or parasympatholytic
drugs. It is important to determine that SND including sinus bradycardia in an individual is not
secondary to cardioactive drugs such as β-blockers or calcium-channel blockers.
FIGURE 63-6 Sinus node dysfunction. A, Sinus bradycardia. Sudden loss of sinus activity (no P waves). Sinus rhythm
resumes after a 4.5-second pause (B), whereas junctional rhythm emerges as a subsidiary mechanism in C. The exact cause
(i.e., sinoatrial exit block versus sinus arrest) cannot be determined from the surface electrocardiogram in these examples. D,
Blocked premature atrial complexes (note distortion of the T wave at arrows compared with sinus cycles) mimic sinus node
dysfunction.
Sinoatrial Exit Block
The sinus node may fire, but the impulse to the atrium can be delayed or interrupted
periodically with loss of P wave (see Fig. 63-6A to C); this abnormality, termed SA exit block,
has been confirmed by intracardiac recordings. Because sinus node activity is not recorded on
the surface ECG, however, the diagnosis of SA exit block is made from analysis of PP intervals.
First-degree SA exit block is difficult to determine from the surface ECG. Diagnosis of second-
degree SA block (type I, II, and higher degrees) can be established more easily. In type I SA
block (SA Wenckebach or Mobitz type I), the PP interval progressively shortens after a pause
(reflecting the dropped P wave), then the cycle repeats. In Mobitz type II or type II second-
degree SA block, a sudden absence of an expected P wave is noted, and the pause is a
multiple of the dominant PP cycle. With a higher degree of block, two or more P waves may be
missing. A subsidiary pacemaker from the AV nodal junction usually emerges during these
circumstances. Third-degree SA block means complete absence of sinus P waves.
Sinus Arrest
Sudden disappearance of P waves could be due to either SA exit block or cessation of sinus
node pacemaker function. The two are difficult to distinguish unless the resultant PP interval
has a predictable periodicity or is a multiple of sinus PP cycle. SA exit block and sinus arrest
must be distinguished from blocked PACs (see Fig. 63-6D) and sinus arrhythmia. Blocked
PACs are likely to distort the ST-T segment and reset the sinus node so that the PP cycle with
a blocked atrial premature contraction is less than two PP intervals. Sinus arrhythmia, which is
a physiologic variation of PP change, usually follows the respiratory cycle (phasic sinus
arrhythmia). The nonphasic variety may result in an abrupt sinus pause and may be confused
with SND.
Bradycardia-Tachycardia Syndrome
Because SND often represents atrial disease processes (e.g., fibrosis, degeneration,
inflammation), coexistence of atrial tachyarrhythmias with bradycardia is not surprising. When
an atrial tachycardia such as AF is terminated, the underlying rhythm may reveal sinus
bradycardia, SA exit block, or even complete atrial standstill with an escape rhythm from a
lower pacemaker in the AV junction or the HPS.
Atrioventricular Blocks
In a resting state, the normal AV node is capable of conducting 200 impulses per minute. With
facilitation of AV nodal conduction owing to adrenergic stimulation or vagal withdrawal, this rate
can reach 250 impulses per minute and even 300 impulses per minute in exceptional cases.
With rapid atrial tachycardia, atrial flutter, and AF, some degree of AV block (in the AV node) is
expected. Abnormal AV block is defined when some impulses are delayed or do not reach the
ventricle during sinus rhythm or sinus tachycardia.
Electrophysiologic and Electrocardiographic Features
First-Degree Atrioventricular Block (Prolonged Atrioventricular Conduction or Interval with 1:1-QRS

Relationship
The normal PR interval is 120 to 200 msec. Because the PR interval incorporates intra-atrial,
AV nodal, and HPS conduction, it could be prolonged because of conduction delay in any of
these areas. The intra-atrial conduction time, which contributes to the PR interval, can be
estimated from the onset of the P wave on the surface ECG to the onset of atrial deflection on
the His bundle electrogram. The AH interval (from the onset of the atrial deflection to the His
bundle potential) represents conduction through the AV node and is normally 60 to 140 msec;
the HPS time estimated by the HV interval (from the onset of the His bundle potential to the
earliest venticular deflection) is 35 to 55 msec. When the PR interval is prolonged, delay is
usually in the AV node (Fig. 63-7A); intra-atrial conduction delays and abnormal HPS
conduction time seldom prolong the PR interval to more than 200 msec and are highly unlikely
to prolong it to more than 300 msec. Block in the AV node or within the His bundle does not
alter the QRS complex morphology compared with sinus rhythm; if a concomitant fascicular or
bundle branch block is noted, infra-His block is likely.
FIGURE 63-7 Atrioventricular (AV) block. A, First-degree AV block (long PR interval). A 3:2 Wenckebach (Mobitz type I)
second-degree AV block is seen in B and Mobitz type II second-degree block in C. Note the PR interval prolongation before the
block in B but no PR increase in C. D, A sudden block of consecutive P waves. No AV conduction following 1:1 AV conduction
with a normal PR interval and right bundle branch block suggests infra-His block. After a long escape interval, a stable
subsidiary pacemaker from the peripheral Purkinje network emerges (idioventricular rhythm).
Second-Degree Atrioventricular Block (Intermittent Atrioventricular Conduction)
With second-degree AV block, some P waves fail to produce a QRS complex. In type I, also
called Mobitz type I or Wenckebach phenomenon, there is a progressive increase in the PR

interval, despite a constant PP rate, until a P wave blocks and the cycle is repeated (see Fig.
63-7B). Any P-to-QRS ratio can be seen (e.g., 3:2, 4:3, 5:4). In a typical Wenckebach
phenomenon, the PR interval after the block is the shortest. The largest increase in PR interval
occurs after the second conducted beat; the R-R interval after the pause, which contains the
blocked P wave, progressively shortens until the next pause. The Wenckebach phenomenon
can be found in all cardiac conducting tissues, but the magnitude of PR prolongation or
shortening from beat to beat is maximum in the AV node and therefore most noticeable. The AV
node is the likely site of block when the PR interval increment with any subsequent PP cycle
exceeds 100 msec, PR shortening is more than 100 msec after the block, or the absolute value
of PR interval with any of the conducted beats is greater than or equal to 300 msec. Most but
not all type I second-degree AV blocks are localized to the AV node.
Type II AV, or Mobitz type II, block causes a sudden, unexpected block of a P wave without a
discernible change in the PR interval before the AV block (see Fig. 63-7C). AV block associated
with marked prolongation of PR interval (i.e., >300 msec) is usually within the AV node, but type
II AV block typically suggests disease in the HPS. When the QRS complex of the conducted
beat is normal or narrow, the block is within the His bundle; an associated bundle branch block
or fascicular block suggests an infra-His site (see Fig. 63-7D). With a normal or only slightly
prolonged PR interval, HPS is a more likely location of block.
A 2:1, 3:1, or higher AV ratio of AV block (Fig. 63-8A) may be noted with progression of Mobitz I
or II to third-degree AV block. The site of block is more difficult to decipher with a 2:1
conduction ratio when the PR and the R wave of the conducted beat are normal.
Documentation of progression from Mobitz type I or II is helpful in determining the site of block.
In the presence of bundle branch block and a normal PR interval, HPS block should be
suspected. Conversely the AV node is the more likely site of block when the PR of the
conducted beat is 300 msec or more because a junctional escape rhythm emerges from a
relatively normal HPS. When the HPS is the site of block, subsidiary pacemakers from a
diseased HPS tend to have a slower escape rate and permit several blocked P waves before
an escape mechanism emerges. In the absence of marked vagal influences, a 3:1 or 4:1 ratio is
seldom noted with AV nodal block during sinus rhythm so that HPS is the more likely site of
block. Vagally mediated AV block is accompanied by concomitant slowing of sinus rate.
FIGURE 63-8 A 2:1 and third-degree block. A, A 2:1 atrioventricular (AV) ratio, a slightly prolonged PR interval of conducted
beats, and right bundle branch block. The site of block is difficult to determine from the surface electrocardiogram (ECG). B and
C, Third-degree block. The escape mechanism has a narrow QRS complex in B at a rate of 50 beats per minute and suggests
intranodal block and a junctional subsidiary pacemaker. The escape mechanism in C is from the peripheral Purkinje network
(idioventricular), as indicated by its slow rate (33 beats per minute) and wide complexes. In both panels, the atrial rates are
constant and unrelated to ventricular rates, which are also constant but driven by a slower subsidiary pacemaker located distal
to the sites of block (AV dissociation). The ECG leads are labeled.
Third-Degree (Complete) Atrioventricular Block (No Atrioventricular Conduction)
Complete failure of impulse propagation along the AV conduction system necessitates

emergence of a subsidiary pacemaker distal to the site of block. Normally, the rate of resting
pacemaker activity is highest in the sinus node (60 to 100 beats per minute), followed by the AV
junction (40 to 60 beats per minute) and the bundle branch–Purkinje system (20 to 40 beats per
minute). When the tissues expected to function as subsidiary pacemakers are abnormal, the
rates may be even slower. During intact AV conduction, all of the subsidiary pacemakers
remain suppressed (overdrive suppression). With abrupt cessation of AV conduction, the first
subsidiary pacemaker response (often referred to as escape beat) is almost always slower than
the subsequent rate from the same subsidiary foci; the rate of the emergent pacemaker below
the site of block gradually accelerates (warm-up phenomenon) to its usual anticipated rate.
When the AV node is the site of third-degree AV block, the AV junctional pacemakers drive the
ventricular rates. The QRS complex morphology is similar to that of sinus beats and normally
warms up to 40 to 60 beats per minute. With infra-His block, the escape rhythm shows a wide
QRS complex, originates distally in the HPS (idioventricular), and has a relatively slow rate.
When the block is within the His bundle and the escape rhythm is also in the His bundle distal
to the block, a narrow QRS complex appears at a slower than expected escape rate because of
the disease process involving the junctional pacemakers.
AV dissociation occurs when the atria and ventricles are driven by different pacemakers. AV
dissociation is generally due to AV or ventriculoatrial block. Complete AV block requires a
subsidiary pacemaker to depolarize the ventricles; in this situation, the P wave is faster than the
QRS complexes, and the two are unrelated (see Fig. 63-8B and C). AV dissociation also occurs
when the rate of subsidiary pacemakers is faster than a normal sinus, such as nonparoxysmal
junctional tachycardia (see Fig. 63-2F) or ventricular tachycardia; if there is retrograde
(ventriculoatrial) block, the atria are driven by the SA node or other atrial pacemakers.
Isorhythmic AV dissociation is the term used when atria and ventricles are driven independently
but have a similar rate.
Clinical Manifestations
Aside from vagal influences and medications such as digitalis and antiarrhythmic drugs, the
exact cause for SND is frequently difficult to determine. The most common causes for SND are
atrial muscle degeneration, fibrosis with advanced age, and cardiac pathology such as coronary
artery disease. Acute inferior wall myocardial ischemia or infarction associated with disease of
the proximal right coronary artery may cause transient SND. Other, less common causes
include acute or chronic inflammation from myocarditis or pericarditis and prior cardiac surgery
with trauma to the sinus node. Congenital SND and complete atrial standstill with no detectable
sinus node activity are seen rarely.
AV nodal blocks can be caused by digitalis, antiarrhythmic drugs, and vagal influences.
Involvement of the AV junctional area with any inflammatory or other disease process can result
in AV nodal block of varying degrees. The most common cause of chronic AV block in the HPS
is progressive fibrosis or calcification in the HPS, or both, with aging or myocardial fibrosis of
any cause. Because of the proximity of aortic and mitral valves to the distal His bundle and
proximal bundle branches, annular calcification or valve surgery can cause acute or chronic
intra-His and infra-His block. Myocardial infiltration by an infectious agent (i.e., Chagas' disease;
Chapter 368) is an important cause of chronic heart block in Latin American countries. Acute
inferior wall ischemia or infarction, or both, can cause various degrees of AV nodal block
because of ischemia in the nodal artery distributions. Involvement of HPS during acute anterior
myocardial infarction can lead to bundle branch block or AV block, or both.
Sinus bradycardia and various degrees of AV nodal blocks are also noted during sleep even in
otherwise healthy people. Asymptomatic first- and second-degree AV block, particularly when
partially or completely reversed by exercise, points toward a benign condition. Persistent
second-degree and third-degree AV nodal block during the waking hours and during activity is
abnormal and is often associated with symptoms of bradycardia, including dizziness, fatigue,
exertional dyspnea, worsening of heart failure, near-syncope, or syncope. Third-degree AV
block with a good junctional escape mechanism that accelerates during exercise, as often
noted in patients with congenital AV block, may remain asymptomatic. Patients with congenital
heart block may not appreciate their potential for a more active lifestyle because of the lack of a
reference point but often feel much better when an appropriate heart rate acceleration can be
achieved after pacemaker therapy.
Bradycardias of all types may be secondary to profound vagal influences, as seen with neurally
mediated syndromes such as vasovagal episodes, vomiting, abdominal surgery, and upper and
lower gastrointestinal invasive procedures. Periods of prolonged sinus arrest and AV nodal
block with marked suppression of subsidiary pacemaker can occur and lead to symptomatic
asystole. Vasovagal (neurocardiogenic) syndromes are a common cause of syncope in
relatively healthy populations (Chapters 61 and 427); in most cases, vasodepression
(hypotension) is the primary cause of syncope, and rate control alone does not relieve
symptoms.
Treatment
Asymptomatic SND or AV nodal block requires no therapy. Acute management of

symptomatic SND and second- and third-degree AV block includes administration of
intravenous atropine (1 mg) or isoproterenol (usually 1 to 2 µg/min infusion) to increase the
heart rate. Temporary cardiac pacing may be needed. When SND or AV block is due to
transient abnormalities, such as drug-induced or acute ischemic syndromes, temporary
pacing is usually sufficient; however, when infra-His or intra-His block is suspected (e.g.,
exercise-induced AV block or asymptomatic Mobitz type II block) and the site can be
documented with His bundle recording, permanent pacing (Chapter 65) is indicated. For all
forms of persistent symptomatic SND or second-degree or third-degree AV block,
permanent pacing is the therapy of choice (Chapter 65). Nevertheless, even prolonged
paroxysmal asystole resulting from a neurocardiogenic mechanism is not an indication for
permanent pacing; instead, pharmacologic therapy that relieves hypotension controls
bradycardiac symptoms as well. As a general rule, bradycardia in individuals younger than
55 is vagal in origin and does not require permanent pacing unless proved otherwise.
Future Directions
Ablation of atrial tissue in or outside the pulmonary veins and atrial defibrillation therapy are
likely to be used more frequently because of technologic advances and patients' preferences,
although it is also conceivable that pharmacologic agents with more targeted effects and fewer
side effects will be developed. Pulmonary vein isolation and ablation to cure AF may become a
first-line therapy. [4]
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Chapter 63CARDIAC ARRHYTHMIAS WITH SUPRAVENTRICULAR ORIGIN fro...

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Goldman: Cecil Medicine, 23rd ed.

Chapter 63 – CARDIAC ARRHYTHMIAS WITH SUPRAVENTRICULAR ORIGIN

Definition and Pathobiology

Supraventricular tachyarrhythmias can occur either as single or consecutive premature

Premature Atrial Complexes

Sustained Supraventricular Tachycardias

TABLE 63-1 -- SUPRAVENTRICULAR TACHYCARDIAS

Sinus Node Re-Entry

Atrioventricular Junctional Tachycardia

Wolff-Parkinson-White Syndrome and Associated Tachycardias

Because the initial QRS activation is due to muscle-to-muscle conduction, as opposed to

Atrioventricular Nodal Re-entry

In the absence of ventricular preexcitation, the most common AV junctional tachycardia is AV

Nonparoxysmal Junctional Tachycardia

Automatic Junctional Tachycardia

See Tables 63-2 and 63-3. See also Chapter 65.

TABLE 63-2 -- SELECTION OF MEDICATIONS FOR SPECIFIC SUPRAVENTRICULAR

TABLE 63-3 -- DRUGS AND DOSES USED TO TREAT SUPRAVENTRICULAR

Long-term anticoagulation therapy with warfarin is generally recommended in all patients

TABLE 63-4 -- BRADYCARDIAS

Sinus bradycardia <45/min

Sinus Node Dysfunction

Sinoatrial Exit Block

Electrophysiologic and Electrocardiographic Features

First-Degree Atrioventricular Block (Prolonged Atrioventricular Conduction or Interval with 1:1-QRS

Second-Degree Atrioventricular Block (Intermittent Atrioventricular Conduction)

called Mobitz type I or Wenckebach phenomenon, there is a progressive increase in the PR

Third-Degree (Complete) Atrioventricular Block (No Atrioventricular Conduction)

Complete failure of impulse propagation along the AV conduction system necessitates

Asymptomatic SND or AV nodal block requires no therapy. Acute management of

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