65
Dysrhythmias
Donald M. Yealy and Joshua M. Kosowsky
KEY CONCEPTS
• E lectrical therapy is appropriate for unstable patients in whom a dysrhyth-
mia is the cause of symptoms—pacing if the heart rate is slow, counter-
shock with sedation if fast.
• Any regular new-­onset, symptomatic, wide-­complex tachycardia should be
assumed to be ventricular tachycardia until proven otherwise.
• Type II second-­degree AV block is never a normal variant and implies a
conduction block below the AV node. When the conduction ratio is 2:1, a
type II block should be assumed until proven otherwise. Pacing should be
readily accessible.
• Any tachycardia exceeding a rate of 225 to 250 beats/min, regardless of
the QRS complex morphology, should be considered an accessory pathway
syndrome. Nodal blocking agents should be avoided.
• Irregularity can be difficult to appreciate in tachycardia over 200 beats/
min. Atrial fibrillation can be missed if R-­R intervals at fast rates are not
carefully tracked.
FOUNDATIONS
Cardiac Cellular Electrophysiology
The term dysrhythmia denotes any abnormality in cardiac rhythm; it
is often used interchangeably with the term arrhythmia. Understand-
ing dysrhythmias begins with understanding the normal electrophys-
iologic function of cardiac cells. Electrophysiology depends on an
intact resting membrane potential, largely the result of differential
concentrations of Na+ and K+ on either side of the cell membrane,
measuring approximately −90 mV in normal resting nonpacemaker
cells. This gradient exists because of the Na+ K+ exchange pump and
concentration-­dependent flow of K+ out of the cell. The influx of Ca2+
through passive exchange with Na2+ also allows for conduction and
myofibril contraction (Fig. 65.1).
In normal nonpacemaker cells, an electrical stimulus causes the
membrane potential to become less negative, termed depolarization.
When the membrane potential reaches −70 mV, specialized Na2+ chan-
nels open, causing a rapid influx of positive charge into the cell. This so-­
called fast channel activity further decreases the membrane potential and
is augmented at 30 to 40 mV by a second slow channel that allows Ca2+
influx. When these channels close, the resting potential is restored by
the sodium-­potassium pump, an event termed repolarization (Fig. 65.2).
In nonpacemaker cells, depolarization from a second electrical
stimulus is not possible when the membrane potential remains more
positive than −60 mV, called the effective refractory period (Fig. 65.3).
When the membrane potential reaches −60 to −70 mV, some fast chan-
nels are capable of responding but impulse propagation is not normal;
this is known as the relative refractory period. At a membrane potential
of −70 mV or less, fast channels are ready for activity (see Fig. 65.3).
890
Pacemaker cells differ from non–impulse-­generating cells in that
they can spontaneously depolarize via slow Na+ influx. Dominant
pacemaker cells are present in the sinoatrial (SA) node, but other pace-
maker cells exist in the atrioventricular (AV) node, within the His-­
Purkinje system, and elsewhere. With a failure of normal pacemaking
cells, or in the setting of other pathologic conditions such as metabolic
derangement or myocardial ischemia, nonpacemaker cells undergo
spontaneous depolarization.
Anatomy and Conduction
The SA node is an area of specialized impulse-­generating tissue at the
junction of the right atrium and the superior vena cava. Its blood sup-
ply is from the right coronary artery (RCA) in 55% of patients and left
circumflex artery (LCA) in 45%. The normal SA node produces spon-
taneous depolarization faster than other pacemakers and is usually the
dominant pacemaker. In healthy adults, the SA node typically main-
tains a rate of 60 to 90 beats/min. Hypothermia and vagal stimulation
slow the sinus rate, whereas hyperthermia and sympathetic stimulation
increase the rate. Low or absent parasympathetic tone—for example,
with certain drugs or after heart transplantation—results in a faster
sinus rate.
In the absence of normal SA node impulses, other myocardial tis-
sues may assume the role of a pacemaker. The AV node has an intrinsic
impulse-­generating rate of 45 to 60 beats/min. Infranodal pacemakers
within the His bundle, Purkinje system, and bundle branches main-
tain intrinsic rates ranging from 30 to 45 beats/min. Under pathologic
conditions, other atrial and ventricular tissues may pace the heart at
varying rates.
Impulses from the SA node are propagated through the atrial tissue
to the AV node. Atrial depolarization is characterized by the P wave on
the surface electrocardiogram (ECG; Fig. 65.4).
The AV node is an area of conduction tissue separating the atria and
the ventricles, located in the posterior-­inferior region of the interatrial
septum. Its blood supply is from a branch of the RCA in 90% of patients
(right dominant) and from the LCA in the remaining 10% (left domi-
nant). Transmission of impulses within the AV node is slower than in
other parts of the conducting system (Table 65.1) because of a depen-
dence on slow-­channel ion influx for membrane depolarization. An
accessory pathway refers to conduction tissue outside the AV node that
forms an alternative, or bypass, tract between the atria and ventricles.
The term preexcitation refers to early ventricular depolarization via an
accessory pathway.
On the surface ECG, the time it takes to conduct an impulse
through the atria to the ventricles is represented by the PR interval,
normally ranging from 0.10 to 0.20 second (see Fig. 65.4). Impulses
originating in lower atrial tissues or accessory pathways often have a
shortened PR interval. PR prolongation is usually a result of nodal or
supranodal conduction system disease.

Na+-Ca2+ exchange
Ca2+
Na+
Na+
K+
Na+, K+-ATPase
exchange pump
K+
Na+
K
Flow of K+ down its
concentration gradient
Fig. 65.1  Flow of various ions across the myocardial cell membrane.
The Na+-­K+ pump exchanges three Na+ ions for each two K2+ ions,
generating a net negative flow of 10 mV. The flow of K down the con-
centration gradient (dark arrow) generates another 80 mV of current.
The Na+–Ca2+ exchange adds little to the resting potential. ATPase,
Adenosine triphosphatase. (From Marriott HJL, Conover MB. Advanced
concepts in dysrhythmias. ed 2. St. Louis: Mosby; 1989.)
After passing through the AV node, impulses propagate to the His
bundle onto the three main bundle branch fascicles—the right bundle
branch (RBB), left anterior-­superior bundle (LASB), and left posterior-­
inferior bundle (LPIB). The RBB and LASB are typically supplied by
the left anterior descending (LAD) artery, whereas the RCA or LCA
may supply the LPIB. After conduction down the three main bundle
branches, impulses are delivered to the Purkinje fibers, propagating
impulses to myocardial tissues in a swift and orderly fashion, allowing
for coordinated ventricular contraction. If an impulse arrives prema-
turely, it may be conducted abnormally (termed aberrant, associated
with bundles that are relatively refractory) or blocked (if the bundles
are entirely refractory).
On the ECG, the QRS complex represents ventricular depolariza-
tion (see Fig. 65.4), normally 0.09 second or less; 0.12 second or longer
is abnormal. The T wave corresponds to ventricular repolarization and
its duration depends, among other things, on the length of the cardiac
cycle. The QT interval represents the total time of ventricular depolar-
ization and repolarization and is altered by inherent physiologic abnor-
malities, metabolic changes, drugs, or structural changes. This interval
is key to assess for QT prolongation in any patient with syncope or
ventricular dysrhythmia, given the link to ventricular dysrhythmia
recurrence.
Mechanisms of Dysrhythmia Formation
Enhanced automaticity refers to spontaneous depolarization in non-
pacemaker cells or depolarization at an abnormally low threshold in
pacemaker cells (Fig. 65.5). Classic examples of enhanced automaticity
include the idioventricular rhythms of severe hyperkalemia or myocar-
dial ischemia and the atrial or junctional tachycardias (JTs) associated
with digoxin toxicity.
Triggered activity refers to abnormal impulse(s) resulting from after-
depolarizations. Afterdepolarizations are fluctuations in membrane
CHAPTER 65  Dysrhythmias 891
potential that occur as the resting potential is restored. These fluc-
tuations may precipitate another depolarization just before the full
resting potential is reached (early afterdepolarizations) or after full
resting potential is reached (delayed afterdepolarizations). The classic
dysrhythmia associated with early afterdepolarization is acquired tor-
sades de pointes, which typically arises in the setting of a prolonged QT
interval and a new metabolic or drug trigger. Delayed afterdepolariza-
tions classically arise in the setting of rapid heart rates and intracellular
Ca2+ overload, as seen with digoxin toxicity or reperfusion therapy for
acute myocardial infarction.
Reentry dysrhythmias arise from repetitive conduction of impulses
through a self-­sustaining circuit (Fig. 65.6). To maintain a reentry cir-
cuit, one conduction pathway must have a longer refractory period
than the other so that when an impulse exits one limb of the circuit,
it may then reenter the other in retrograde fashion. The cycle is then
repeated, creating self-­sustaining dysrhythmia. Reentry mechanisms
are responsible for most regular narrow-­complex tachycardias and
many ventricular tachycardias (VTs). Treatment is predicated on alter-
ing conduction in one or both limbs of the circuit.
CLASSIFICATION OF ANTIDYSRHYTHMIC DRUGS
The four classes of antidysrhythmic medications are categorized
according to their electrophysiologic effects (Box 65.1). Class I agents
exert their major effects on the fast Na+ channels, resulting in mem-
brane stabilization. The subclasses IA, IB, and IC have differing effects
on depolarization, repolarization, and conduction. Class II agents
are the β-­adrenergic antagonists, which depress SA node automatic-
ity, slow AV node conduction, and suppress conduction in ischemic
myocardial tissue. Class III agents prolong repolarization and refrac-
tory period duration, predominantly via their effects on K+ channels.
Class IV agents are the Ca2+ channel blockers, which slow conduction
through the AV node and suppress other calcium-­dependent dysrhyth-
mias. Other agents important in the emergency treatment of dysrhyth-
mias include magnesium sulfate, digoxin, and adenosine.
Class IA Agents
Class IA agents slow conduction through the atria, AV node, and His-­
Purkinje system and suppress conduction in accessory pathways. As
such, they slow both depolarization and repolarization. Class IA agents
also exhibit anticholinergic and mild negative inotropic effects.
Procainamide
Procainamide is the only class IA agent commonly used in the emer-
gency treatment of ventricular and supraventricular dysrhythmias,
and it can alter normal and accessory pathway conduction. In stable
patients, the recommended administration is a rate of 20 to 30 mg/min
until the dysrhythmia is terminated, hypotension occurs, or the QRS
complex widens (to 50% of the pretreatment width), up to a total dose
of 18 to 20 mg/kg (12 mg/kg if congestive heart failure is present). Pro-
cainamide triggers hypotension from vasodilatory effects in 5% to 10%
of patients and may be associated with or worsened by infusion rate.
It is the preferred agent in treating Wolff-Parkinson-White syndrome.
Class IB Agents
Class IB agents slow conduction and depolarization less than other
class I agents, and they shorten repolarization rather than prolonging
it. Class IB agents have little effect on accessory pathway conduction.
Lidocaine
Lidocaine is the sole class IB agent used in emergency rhythm man-
agement. Lidocaine can suppress dysrhythmias from enhanced
892 PART III  Emergency Medicine by System

Overshoot Plateau Repolar-

+ 20 phase ization

0 Time
1 2

Depolarization
–20

Millivolts
0
–40
3
–60 Membrane Restoration
resting of ionic
–80 potential balance
–90
4 4
Intracellular K+
fluid space K+
ATP
Sarcolemma ADP +

K+
N
Na+ Ca2+

a
Extracellular

+
A fluid space

SA node

Atria
1 2
0 3
AN 4
SA
1 2
AV node

N 0 3
4
NH
NH 1
2

0 3
His bundle
4
H
Purkinje
fiber
1
2
100 mV

Ventricles 0
4 3
BB
B 200 msec C
Fig. 65.2  (A) Action potential of a myocardial cell and its relation to ion flow. (B) Action potentials of various
myocardial tissues. (C) Action potentials of various pacemaker cells. Note that phase 4 becomes flatter as
its location becomes more distal. AN, Atrial-­nodal; AV, atrioventricular; BB, bundle branch fascicles; H, His
bundle; N, nodal; NH, nodal-­His; SA, sinoatrial. ([A and B] From Calcium in cardiac metabolism, Whippany,
NJ, 1980, Knoll Pharmaceutical; and [C] from Conover M. Understanding electrocardiography. ed 5. St Louis:
Mosby; 1988.)

Supernormal refractory period Class IC Agents

Relative refractory period
The class IC agents profoundly slow depolarization and conduction.
+ 20
More than any other class, these agents are associated with prodys-
0 Time
1 2 rhythmia, the creation of a new dysrhythmia; this potential new dys-
–20 rhythmic event also exists with class IA agents albeit much less than
Millivolts

Effective
–40 0 (absolute) class IC. Class IC agents are approved for oral use in the United States.
refractory 3
–60 period
–65 Threshold Flecainide
–80 potential
–90 Flecainide is a class 1C antidysrhythmic agent used for paroxysmal
4 4 supraventricular tachycardia and certain forms of VT. Flecainide
Fig. 65.3  Action potential showing various refractory periods. (From Cal- has high oral bioavailability, variable half-­life, and narrow therapeu-
cium in cardiac metabolism, Whippany, NJ, 1980, Knoll Pharmaceutical.) tic index, all hampering its use. Flecainide is not recommended for
patients with ischemic or structural heart disease.
automaticity, such as VT. Lidocaine also suppresses SA and AV node
function and is associated with asystole in the setting of acute myo- Propafenone
cardial ischemia. Lidocaine is an alternative to amiodarone but has no Propafenone shares electrophysiologic properties with classes IA and IC
efficacy in SVT. agents and possesses some β-­adrenergic and calcium channel-­blocking
 CHAPTER 65  Dysrhythmias 893

properties. Oral propafenone is used to prevent atrial fibrillation and
ventricular dysrhythmias. Like flecainide, propafenone is used with
caution in patients who have ischemic or structural heart disease.
Class II Agents
Class II agents—β-­adrenergic blockers—suppress SA node automatic-
ity and slow conduction through the AV node. Because of their effect
on AV node conduction, class II agents are well suited to control the
SA node
ventricular rate in patients with atrial tachydysrhythmias and can be
useful to terminate AV nodal reentrant tachycardias (AVNRTs). In the
setting of acute myocardial ischemia, beta blockers may lessen the fre-
quency of ventricular dysrhythmias.
All beta blockers are active at β1 and β2 receptors (Table 65.2) to
varying degrees; those with more prominent β1 effects are called car-
dioselective. Relative contraindications to the use of beta blockers
include advanced congestive heart failure and third-­trimester preg-
nancy. Historically, beta blockers have been avoided in patients with
asthma and chronic obstructive pulmonary disease. However, car-
dioselective beta blockers are not associated with an increased risk of
asthma or chronic obstructive pulmonary disease (COPD) exacerba-
tions.1 Beta blockers should not be used in patients with preexisting
bradycardia or heart block beyond first-­degree. Acute side effects of
beta blockers include heart failure, excessive bradycardia, and hypoten-
sion. In rare cases, they may cause bronchospasm, but most instances
are not clinically apparent. Intravenous (IV) beta blockers can trigger
additive side effects when used in conjunction with calcium channel
blockers, notably hypotension or bradycardia. Only two beta blockers
are commonly used in emergency care of dysrhythmias.

Esmolol
Esmolol is an intravenous β1-­selective agent useful in the emergency
setting because of its rapid onset of action and short elimination half-­
life (minutes). Common dosing of esmolol is an IV bolus of 500 μg/
kg followed by a continuous infusion beginning at 50 μg/kg/min and
titrating to need and effect.

Normal values Metoprolol

SP = 34.9 ± 2.1 msec Metoprolol is available in oral and IV preparations. Although not
PA = 37 ± 7 approved for dysrhythmia treatment in the United States, metoprolol
ECG AH = 77 ± 16
HV = 40 ± 3 (5 to 10 mg IV every 10 to 15 minutes in an adult, titrated to response)
will slow atrial and nodal tachycardias.

Class III Agents

All class III agents prolong the refractory period primarily by blocking
K+ channels, with variable effects on the QT interval. In general, class

HBE
TABLE 65.1  Conduction Velocities in
A H
V Various Heart Tissues
Fig. 65.4  Electrical events in the heart related to surface electrocardio- Tissue Velocity (m/s)
gram (ECG) and His bundle electrogram (HBE). The approximate rela-
Atrium 1000
tionship of sinus node discharge is also related to the surface ECG.
AH, Atrioventricular nodal conduction time; HV, His-­Purkinje conduction; Atrioventricular node 200
PA, intra-­atrial conduction time; SA, sinoatrial; SP, SA conduction time. His-­Purkinje system 4000
(From Marriott HJL, Conover MB. Advanced concepts in dysrhythmias. Ventricles 400
ed 2. St. Louis: Mosby; 1989.)

0 mV 0 mV

TP

A –90 mV B –90 mV
Fig. 65.5  (A) Enhanced normal automaticity (dashed line). (B) Abnormal automaticity. TP, Threshold point.
(From Marriott HJL, Conover MB. Advanced concepts in dysrhythmias. ed 2. St. Louis: Mosby; 1989.)
894 PART III  Emergency Medicine by System

III agents are alternatives to class I agents for the treatment of many
ventricular and atrial dysrhythmias.
Amiodarone
Amiodarone is approved for the treatment of ventricular and supra-
ventricular dysrhythmias and is a first line drug treatment for acute
ventricular tachycardia. In addition to features in common with all
class III agents, amiodarone has other effects, including actions similar
to those of class IA, II, and IV agents.
The serum half-­life of amiodarone is 9 to 36 days after a single
IV dose and up to 107 days during long-­term oral use. Because of its
unusual pharmacokinetics, oral regimens vary widely. The acute side
effects of amiodarone include hypotension, bradycardia, and heart
failure (Box 65.2). There is an additive risk of bradycardia and hypo-
tension when amiodarone is used in conjunction with calcium chan-
nel or β-­adrenergic blockers. Rates of prodysrhythmia are relatively
A B
low. Long-­term amiodarone use may create extracardiac side effects,
including both reversible and irreversible lung and thyroid disease.
Amiodarone alters the pharmacokinetics of numerous other drugs,
including digoxin and warfarin.
Ibutilide
Ibutilide is a parenteral agent that induces a slower inward Na2+ cur-
rent, prolonging the refractory period. IV ibutilide approved indi-
cations include cardioversion of atrial fibrillation and atrial flutter.
Because of QT prolongation and the risk of polymorphic VT, we rec-
ommend to start ibutilide with continuous cardiac rhythm monitoring.
Sotalol
Sotalol is an oral β-­adrenergic receptor blocker with type III antidys-
rhythmic properties. Uses are for the suppression of supraventricular
and ventricular dysrhythmias. Like ibutilide, sotalol initiation is best
with cardiac monitoring setting, watching for QT prolongation; it has a
very limited role in emergency care.

A Dofetilide
Dofetilide is a powerful class III agent approved for chemical cardio-
version and maintenance of sinus rhythm in patients with atrial fibril-
lation or flutter. However, because of its high risk for prodysrhythmia,
X it is used sparingly and prescribed by physicians with specialized train-
X
ing. It has no current role in emergency care.

Dronedarone
Structurally related to amiodarone, dronedarone displays class III
A B C B properties in addition to those of other antidysrhythmic classes. Drone-
Fig. 65.6  Mechanism of reentry. darone is approved for oral use to maintain sinus rhythm in patients

BOX 65.1  Classification of Antidysrhythmic Drugs

Class I Class II
Sodium (fast) channel blockers—slow depolarization with varying effects on β-­Adrenergic blockers
repolarization. These drugs have membrane-­stabilizing effects. Propranolol
Esmolol
Class IA Metoprolol
Moderate slowing of depolarization and conduction; prolong repolarization and Atenolol
action potential duration.
Procainamide Class III
Quinidine Antifibrillatory agents—prolong action potential duration and refractory period
Disopyramide duration with antifibrillatory properties.
Bretylium (historical significance)
Class IB Amiodarone
Minimally slow depolarization and conduction; shorten repolarization and action Dofetilide
potential duration. Ibutilidea
Lidocaine Sotalolb
Phenytoin Dronedarone
Tocainide Azimilide
Mexiletine
Class IV
Class IC Calcium (slow) channel blockers
Markedly slow depolarization and conduction; prolong repolarization and action Verapamil
potential duration. Diltiazem
Flecainide
Propafenone (shares properties with class IA agents) Miscellaneous
Vernakalant (atrial-­specific, investigational) Digoxin
Magnesium sulfate
Adenosine
a Shares activity with class I agents.
b Shares activity with class II agents.
 CHAPTER 65  Dysrhythmias 895

TABLE 65.2  Cardiac and Respiratory β-­Adrenergic Receptors and Responses to Pharmacologic
Manipulation
Response to Receptors Location Stimulation Antagonism
β1-­Adrenergic Heart Increased heart rate and ectopy Decreased heart rate and ectopy
Increased contractility Decreased contractility
β2-­Adrenergic Airway (smooth muscle) Decreased tone (relaxation) Increased tone (contraction)
Peripheral vasculature Decreased tone (relaxation) Increased tone (contraction)

BOX 65.2  Adverse Effects of Amiodarone

Verapamil
Acute Effects Verapamil is rarely used in emergencies, although it is effective. A start-
Hypotension ing dose of 0.1 mg/kg IV over 1 to 2 minutes; for the average healthy
Slowing of heart rate adult, this translates to a dose of 5 to 10 mg, which can be repeated
Decreased contractility or increased by 50% if unsuccessful and there is no hypotension 10
minutes after administration. In older adults or those with border-
Long-­Term Effects line hypotension (systolic blood pressure of 90 to 110 mm Hg), use a
Common Effects smaller dose (0.05 mg/kg IV or 2.5 mg increments).
Corneal deposits
Photosensitivity Miscellaneous Agents
Gastrointestinal intolerance Adenosine
Adenosine is a naturally occurring purine nucleoside used to termi-
Less Common Effects
nate regular, nonatrial, narrow-­complex tachydysrhythmias, notably
Hyperthyroidism
junctional reentry. Administered as an IV bolus, adenosine causes an
Heart failure
abrupt slowing of AV conduction in anterograde and retrograde path-
Pulmonary toxicity, fibrosis
ways. Adenosine has an onset of action of 5 to 20 seconds and a dura-
Hypothyroidism
tion of effect of 30 to 40 seconds. Except in rare cases, adenosine has
Bradycardia
little or no effect on infranodal conduction pathways. For this reason,
Prodysrhythmic effect
adenosine is an option as a diagnostic (and sometimes therapeutic)
Blue-green skin discoloration
agent in patients with wide-­complex tachydysrhythmia when the spe-
Drug Interactions cific rhythm is unclear. Patients with transplanted hearts are very sen-
Increased Levels sitive to adenosine and may have profound nodal block.
Phenytoin Start adenosine by using a 6-­mg rapid IV bolus (through a large,
Procainamide non–distal vein followed by a rapid flush) for adults (≥50 kg body
Warfarin mass); one key to success is the rapid bolus adherence. If no response is
Digoxin seen within 1 to 2 minutes, increase the dose to a 12-­mg rapid IV bolus.
Flecainide If no effect is seen after a second 12-­mg dose, then reassess the rhythm
and use another therapy. There is no benefit to repeating adenosine
when transient lowering of the heart rate occurs after a dose is given,
with atrial fibrillation or flutter but is contraindicated in patients with followed by a return to the previous rhythm. Pediatric doses are 0.05
severe or recent heart failure. It has no current role in emergency care. mg/kg initially, with doubling at similar intervals, up to a total dose of
0.25 mg/kg. Heart transplant patients should receive 0.025 mg/kg, for
Class IV Agents starting doses of 1.5 to 3 mg.2
Class IV agents block slow Ca2+ channels, slowing conduction within Side effects occur in up to one-­third of patients given adenosine
the AV node and suppressing the SA node to a lesser degree. Like beta but are usually minor and self-­limited. These include flushing, dyspnea,
blockers, these are used in patients with supraventricular tachycardia. chest pressure, nausea, headache, dizziness, transient bradycardia or
All class IV agents are associated with peripheral vasodilation. Ver- heart block, sense of impending doom, and hypotension. Asystole is
apamil has the least effect on peripheral vascular tone, and diltiazem possible but generally transient.
has an effect between that of verapamil and purely peripherally acting Because of its short duration of action, adenosine is not an effective
calcium channel blockers (e.g., nifedipine). Both agents can be given rate-­control agent for atrial fibrillation or flutter, although it can help
orally after IV use if needed. Class IV drugs are should be avoided in unmask these rhythms when not apparent on the initial surface ECG.
patients with second-­or third-­degree AV block unless the patient has
an external pacemaker. Class IV drugs may cause excessive bradycardia Digoxin
in those with first-­degree AV block. Digoxin compounds have a variety of effects on myocardial cells: They
inhibit the adenosine triphosphate (ATP)–dependent Na+-­K+ exchange
Diltiazem pump, increasing intracellular Na+ concentrations, and decrease intra-
IV diltiazem dosing is a 0.25 to 0.35 mg/kg bolus over 2 minutes. For cellular K+ concentrations. The resultant increase in intracellular Ca2+
longer-­term rate control, a continuous infusion (5 to 15 mg/hr IV ini- concentration accounts for the positive inotropic effects of digoxin.
tially, then titrated to need) or an oral dose (60 to 90 mg immediate-­ The prodysrhythmic effects of digoxin are enhanced automaticity and
release formulation initially) will sustain the response. triggered activity, particularly at high therapeutic or toxic doses. At the
896 PART III  Emergency Medicine by System
BOX 65.3  Adverse Effects of Digoxin
Common Effects
Gastrointestinal intolerance (e.g., nausea, vomiting, abdominal pain, diarrhea,
anorexia)
Fatigue
Drowsiness
Headache
Depression
Apathy
Less Common Effects
Psychosis
Cardiac symptoms
Heart block
Increased ectopy
Combined block and ectopy (multifocal atrial tachycardia with block or com-
plete atrioventricular block with accelerated junctional rhythm, usually in
the overdose setting)
Ventricular tachycardia
Visual color disturbances
same time, digoxin slows AV node conduction via lengthening of the
refractory period. Classic (albeit not common) digoxin toxicity shows
signs of both enhanced excitability and slowed conduction (rapid atrial
activity with slow ventricular responses or AV block.)
Digoxin (0.25 to 0.5 mg IV) can control the ventricular rate in
patients with supraventricular tachycardia, notably atrial fibrillation
and atrial flutter. Because of its slower onset of action (often not ther-
apeutic for 30 minutes or longer and peaking at 6 hours), digoxin is
not a first-­line agent for emergency therapy. However, digoxin can be
beneficial in the acute treatment of dysrhythmias in patients with car-
diogenic shock or heart failure.
Side effects of digoxin are listed in Box 65.3 and are aggravated by
hypokalemia, hypercalcemia, hypomagnesemia, increased catechol-
amine levels, and acid-­base disturbances. Digoxin toxicity is discussed
in Chapter 147.
Magnesium
Magnesium can abort ventricular dysrhythmias via its membrane-­
stabilizing properties. Magnesium (1 to 2 g IV) may terminate torsades
de pointes and is an adjunct in ventricular tachycardia therapy.
Isoproterenol
This non-­selective beta-­adrenergic agonist is used to treat some brady-
cardic patients—notably those with denervation like post-­heart trans-
plantation—or to prevent acquired torsades de pointes recurrence in
some cases of beta-­blocker overdose. It directly stimulates beta-1 and
beta-2 receptions, speeding SA and AV activity and enhancing contrac-
tility while relaxing vascular and other smooth muscles. It may increase
heart rate, but blood pressure effects vary by the relative impact on car-
diac output (increase) and vasodilation (decrease). Administration is
via IV bolus if needed (1 to 2 mcg), but more commonly by IV infusion
(2 to 10 mcg/minute titrated to effect).
Clinical Features
Dysrhythmias are classified according to their electrophysiologic ori-
gin, appearance on the ECG, and underlying ventricular rate. Although
overlap exists, the following categorization is useful:
• Bradycardias
• Extrasystoles
• N arrow-­complex (QRS < 0.12 second) tachycardias (regular and
irregular)
• Wide-­complex (QRS ≥ 0.12 second) tachycardias (regular and
irregular)
The clinical approach to a patient with suspected dysrhythmia starts
with assessing clinical stability, which is driven by the effect on perfu-
sion. Unstable patients have severe or multiple end-­organ features of
hypoperfusion, such as altered sensorium, respiratory distress, hypo-
tension, syncope, or chest pain suggestive of myocardial ischemia.
Stable patients may be asymptomatic or have mild symptoms, such as
lightheadedness, dyspnea on exertion, palpitations, or mild anxiety. In
practice, clinical stability is a continuum; in the absence of profound
altered sensorium or hypotension, distinguishing stable and unsta-
ble patients with precision is often not possible. One simple axiom is
important:
• Unstable patients with a dysrhythmia outside of a clear external
trigger (e.g., bradycardia for hypothermia or tachycardia for hypo-
volemic or distributive shock) need prompt electrical therapy—a
countershock if there is a fast rate with a pulse, or cutaneous pacing
if there is a slow rate with a pulse. Care of patients with cardiac
arrest (i.e., those with no pulse) is discussed in Chapter 8.
A key consideration is whether dysrhythmia is the cause or effect
of a clinical presentation; for example, rapid atrial fibrillation may
cause hypotension or may be a response to volume depletion. Failure
to consider the clinical situation can harm a patient (e.g., giving a rate-­
slowing agent when the tachycardia is a response to hypovolemia).
Thus, the most important decision is often whether dysrhythmia is
likely the primary cause of instability. When there does not appear to
be another cause, treating the dysrhythmia as primary is appropriate.
In a stable patient, a more systematic approach allows identifying the
cause and choosing the most appropriate therapy.
Initial Assessment of Stable Patients
The approach begins with gathering evidence from the history, physi-
cal examination, and 12-­lead ECG with a rhythm strip. The symptom
characteristics are important, including the timing, velocity of onset
(gradual vs. abrupt), and duration. For patients with palpitations, clini-
cians should ask about the rate and regularity of the heartbeat or have
the patient tap out the rhythm with a finger. Other important ques-
tions include precipitating events and associated symptoms, such as
dizziness, chest pain, dyspnea, or syncope. A history of rhythm distur-
bances, ischemic or structural heart disease, and the medication his-
tory may raise a concern for specific rhythms. For example, a new and
symptomatic wide-­complex tachycardia in a patient with known isch-
emic heart disease is much more often VT than a supraventricular dys-
rhythmia. Occasionally, the family history helps, particularly if there
are first-­degree relatives with a history of dysrhythmia, unexplained
syncope, or sudden death—all of which suggest an inherited disorder,
such as an accessory pathway or Brugada syndrome.
Aside from palpating the pulse and listening to the heart sounds,
the physical examination should be focused on detecting evidence of
end-­organ hypoperfusion or clues to an underlying cause of the dys-
rhythmia (e.g., left ventricular failure or thyromegaly). Observing
the patient’s rhythm on a continuous cardiac monitor while he or she
reports symptoms can determine if symptoms link to electrocardio-
graphic findings.
Differential Diagnosis
Loose leads, muscle contraction, shivering, tremors, and other move-
ments can produce artifactual findings on a monitor, rhythm strip,
or 12-­lead ECG (Fig. 65.7). Such pseudodysrhythmias mimic serious
dysrhythmias, including ventricular fibrillation. One should avoid
 CHAPTER 65  Dysrhythmias 897

II

V1

V5

Fig. 65.7  Pseudodysrhythmia. In this case, atrial flutter waves appear to be present but are recognized as an
artifact when the patient and right side of the electrocardiogram are examined.

I aVR V

II aVL V

III aVF V

Fig. 65.8  Note the P waves before the QRS complexes in lead aVF.

decisions based solely on the ECG without incorporating the clinical

context. BOX 65.4  Basic Electrocardiographic
The 12-­lead ECG is essential to evaluating any patient with a sus- Observations During Dysrhythmia Analysis
pected dysrhythmia. The use of a single ECG lead is often adequate
1. Ventricular rate—fast (>100 complexes/min), slow (<60 complexes/min),
for diagnosis, especially in unstable patients; multiple leads are optimal
or normal (60–100 complexes/min).
in stable patients. The latter helps detect the presence or absence of P
2. Rhythm—regular, completely irregular (irregularly irregular or chaotic),
waves (often best seen in inferior leads or V1-2; Fig. 65.8), the relation-
regular with occasional irregularity, or grouped impulses; calipers, long strips
ship between P waves and QRS complexes, prolongation of the QRS
help detect subtle irregularities
and QT interval, and evidence of ischemia or prior myocardial infarc-
3. QRS width—prolonged (>0.12 s), borderline (0.09–0.12 s), or normal. If
tion (Box 65.4). For certain conditions, such as Brugada syndrome, the
determined without electrocardiogram being physically present (e.g., pre-
12-­lead ECG, together with a history of syncope, is diagnostic. Because
hospital radio medical command), ask for QRS duration in “number of small
useful information about paroxysmal dysrhythmias occurs at the onset
boxes” from printed rhythm strip (each box = 0.04 s) to ensure accuracy.
or termination of the rhythm, inspect those areas carefully and save the
4. P wave presence and relationship to QRS complexes—May require map-
strip(s) for future reference.
ping of P waves with calipers to detect those falling within QRS complex or
Vagal maneuvers, such as carotid sinus massage and the Valsalva
T wave.
maneuver, increase parasympathetic tone through the vagus nerve to
5. Rhythm changes—examine these areas closely for clues.
transiently slow AV conduction, which may help uncover or terminate
6. Multiple leads, especially chest leads or esophageal lead if difficulties with
a supraventricular rhythm disturbance. In the ED, these maneuvers
P wave visualization are experienced.
often fail, likely from a selection bias (easy responders terminate before
7. Comparison with previous tracings (if available) is often valuable.
arrival) or ineffective technique. The key to using physical methods of
898 PART III  Emergency Medicine by System
I aVR
II aVL
III aVF
Fig. 65.9  Sinus bradycardia.
enhancing parasympathetic tone is to optimize technique—have the
patient lie flat, lift the legs, and ask for a Valsalva effort, with or with-
out massage, to enhance success. A nodal reentrant tachycardia may
terminate abruptly with vagal maneuvers, whereas it often temporarily
slows the ventricular rate in those with atrial fibrillation or atrial flut-
ter; ventricular tachycardia patients rarely have any change after vagal
maneuvers. Vagal maneuvers are frequently unsuccessful in the ED
but rarely result in clinical deterioration. Auscultate the neck for bruits
before carotid sinus massage, particularly in older patients, and avoid
the maneuver if any are found or preexisting carotid disease is likely.
Other vagotonic maneuvers, such as rectal or ocular massage and ice
water head dunking, are impractical and less effective.
MANAGEMENT
Sinus Bradycardia and Sinoatrial and Atrioventricular
Block
Bradycardia is defined as a ventricular rate of less than 60 beats/min,
although in practice, rates above 50 beats/min are not usually a con-
cern. Bradycardia occurs because of depression of the sinus node or
because of a conduction system block; when the rate falls below a
threshold, a subsidiary pacemaker elsewhere in the atrium, AV junc-
tion, or ventricle may assume the dominant role, resulting in an escape
rhythm.
Sinus Bradycardia
Sinus bradycardia shows an ECG with a P wave assuming normal mor-
phology, a fixed P-­P interval equal to the R-­R interval, and a ventric-
ular rate below 60 beats/min (Fig. 65.9). This pattern may be found
in healthy individuals, particularly well-­conditioned athletes or young
adults with a high resting vagal tone. Sinus bradycardia occurs in a vari-
ety of pathologic conditions associated with vagal stimulation, rang-
ing from autonomic-­mediated syncope to hemoperitoneum or acute
inferior wall myocardial infarction. Other pathologic causes of sinus
bradycardia include hypothermia, hypoxia, drug effects (especially
β-­adrenergic blockers and calcium channel blockers), and intrinsic
sinus node disease (i.e., sick sinus syndrome). When sinus bradycardia
drops below 40 beats/min, a junctional escape rhythm may emerge.
Sinus bradycardia is usually asymptomatic and requires no spe-
cific treatment. If needed, first-­line treatment for symptomatic sinus
bradycardia in adults is atropine, 1 mg IV every 3 to 5 minutes, to a
total dose of 3 mg. Rarely, dopamine or epinephrine infusion may
V1 V4
V2 V5
V3 V6
be administered. Emergency cutaneous pacing for sinus bradycardia
is rarely indicated. In the post-­heart transplant patient, use an iso-
proterenol infusion (2 to 10 mcg/min titrated to effect) as atropine is
ineffective.
Sinus Dysrhythmia
Sinus dysrhythmia is a manifestation of the natural variation in heart
rate that occurs during the respiratory cycle, manifested on the surface
ECG as normally conducted P waves with a variable P-­P interval (Fig.
65.10). It is a normal variant and frequent in children and young adults.
Sinus Arrest and Sinoatrial Exit Block
A lack of atrial depolarization occurs because of failure of the sinus
node to generate an impulse (sinus arrest) or failure of impulse con-
duction out of the SA node (SA exit block; Fig. 65.11). With SA exit
block, it is not uncommon to see dropped P waves in regularly occur-
ring patterns, representing 2 : 1, 3 : 1, or 4 : 1 block. Sinus arrest and SA
exit block may be from intrinsic SA node disease but can occur with
increased vagal tone, whether benign or pathologic. When symptom-
atic, the approach to treatment is similar to that for sinus bradycardia.
Sick Sinus Syndrome
Sick sinus syndrome (SSS) is a group of dysrhythmias caused by dis-
ease of the sinus node and its surrounding tissues, creating sinus bra-
dycardia, sinus arrest, or SA exit block. A variant of SSS known as
bradycardia-­tachycardia syndrome is characterized by one or more of
these bradydysrhythmias alternating with a tachydysrhythmia, typi-
cally atrial fibrillation. SSS is most common in older adults, a result
of fibrotic degeneration. It is associated with cardiomyopathies, con-
nective tissue diseases, and certain drugs. In the acute setting, the spe-
cific rhythm should be treated, although subsequent bradycardia could
require temporary pacing following the use of a nodal blocking agent
(especially a calcium channel blocker) for the tachycardic presentation.
Long-­term management requires permanent pacemaker placement for
symptomatic bradycardia to allow for pharmacologic therapy for atrial
fibrillation.
Atrioventricular Block
AV block results from impaired conduction through the atria, AV
node, or proximal His-­Purkinje system. First-­and second-­degree AV
blocks represent partial impairment of conduction, whereas third-­
degree block indicates complete interruption. Advanced or high-­grade

I aVR
II aVL
III aVF
Fig. 65.10  Sinus dysrhythmia (note slight irregularity).
V1
B
Fig. 65.11  (A) Incomplete sinus block. (B) Complete sinus block (sinus arrest) with ventricular escape rhythm.
AV block refers to AV block resulting in a ventricular rate that is patho-
logically slow.
First-­Degree Atrioventricular Block
First-­degree AV block is from prolonged conduction at the level of the
atria, AV node (most common), or His-­Purkinje system. On the ECG,
first-­degree AV block shows a prolonged PR interval (>0.20 second),
typically with a narrow-­QRS complex (Fig. 65.12). First-­degree AV
block is a normal variant in up to 2% of healthy young adults. First-­
degree AV block requires no specific treatment other than avoiding
nodal blocking agents.
Second-­Degree Atrioventricular Block
Second-­degree AV block is when one or more (but not all) atrial
impulses fail to reach the ventricles. The conduction ratio is the num-
ber of P waves to the number of QRS complexes over a period (e.g.,
3 : 2, 2 : 1). When the atrial rate is unusually fast, such as with atrial flut-
ter, a conduction ratio of 2:1 may be physiologic, reflecting the normal
refractory period of the AV node. However, in most other cases, a con-
duction ratio greater than 1:1 is pathologic. Second-­degree AV block is
CHAPTER 65  Dysrhythmias 899
V1 V4
V2 V5
V3 V6
classified into two types based on the underlying pathophysiology and
appearance of the ECG (Table 65.3).
Type I Second-­ Degree Atrioventricular Block. Type I second-­
degree AV block, also called Wenckebach or Mobitz I AV block, is
associated with progressive impairment of conduction within the AV
node. The surface ECG shows a lengthening of the PR interval from
beat to beat until a P wave fails to conduct to the ventricle (so-­called
dropped beat). This pattern gives the appearance of successive P waves
retreating into the preceding QRS complexes (Fig. 65.13). Grouped
beating (e.g., pairs, trios) occurs but is not unique to type I second-­
degree AV block (Box 65.5).
Type I second-­degree AV block occurs in a variety of conditions,
benign and pathologic; often, these are associated with increased vagal
tone and do not require specific treatment. In the setting of acute myo-
cardial infarction, type I second-­degree AV block is generally transient
and associated with a good outcome.
Type II Second-­Degree Atrioventricular Block. Type II second-­
degree AV block, or Mobitz II block, is a conduction block just below
the level of the AV node. On the surface ECG, conduction of atrial
impulses is sporadic and typically periodic, but the PR interval does
900 PART III  Emergency Medicine by System

Fig. 65.12  First-­degree atrioventricular block.

rhythm pacemaker. Pacemakers above the His bundle often have a

TABLE 65.3  Features of Types I and II
narrow-­QRS complex at a rate of 45 to 60 beats/min, whereas pace-
Second-­Degree Atrioventricular Block makers at or below the His bundle produce a wide-­QRS complex at a
Feature Type I Type II rate of 30 to 45 beats/min.
The hallmark of complete heart block is AV dissociation (i.e., no
Clinical Usually acute Often chronic
electrocardiographic relationship between P waves and QRS com-
Inferior myocardial infarction Anteroseptal
plexes), with an R-­R interval longer than the P-­P interval. Conversely,
Rheumatic fever Lenègre disease the presence of AV dissociation with an R-­R interval shorter than the
(Lev disease) P-­P interval (e.g., as occurs with accelerated junctional rhythms and
Digoxin or beta blockers Cardiomyopathy VTs) does not imply third-­degree heart block. When the atrial rate
Anatomic Usually AV node Infranodal and the escape rates are similar (termed isorhythmic), detecting AV
Electrophysiology Increased relative refractory No relative refractory dissociation may require a long rhythm strip to track the P waves and
period period QRS complexes. When a complete heart block occurs in the presence
of atrial fibrillation, the fibrillatory atrial waves are accompanied by
Decremental conduction All or none conduction
a slow and regular ventricular response (so-­called regularized atrial
Electrocardiographic RP/PR reciprocity PR interval stable
fibrillation). This specific dysrhythmia is classically associated with
features Prolonged PR interval PR interval usually digoxin toxicity.
normal Third-­degree AV block can be congenital but is usually acquired
QRS duration normal QRS duration because of senescent degeneration of the electrical conduction system
prolonged or as a result of acute ischemia, drug therapy, or other pathologic con-
Response to atropine Improves Worsens ditions (e.g., Lyme or Chagas’ disease).
and exercise In the ED setting, management of type II second-­degree or third-­
Response to carotid Worsens Improvesa degree block depends on the cause and presence of symptoms. Symp-
massage tomatic patients with signs of hypoperfusion at rest should be treated
with temporary transcutaneous or transvenous pacing, while revers-
AV, Atrioventricular. ible causes (e.g., ST-­ elevation myocardial infarction, beta-­ blocker
aPrimarily refers to conduction ratio.
overdose) are sought and treated. These patients require cardiology
consultation for consideration of a permanent pacemaker. Atropine is
not widen from beat to beat (Fig. 65.14). The QRS complex is usually usually ineffective; it should be avoided, particularly when the cause of
narrow, but concomitant infranodal conduction disturbances (i.e., the block is acute myocardial ischemia.
bundle branch blocks) can be seen in those with type II second-­degree
AV block. Extrasystoles
When the conduction ratio is exactly 2 : 1, it is hard to distinguish An extrasystole is an electrical impulse originating from an ectopic
type I from type II second-­degree AV block on the surface ECG. In gen- atrial or ventricular focus. Depending on the site of origin and timing
eral, a prolonged PR interval makes type I block more likely, whereas of the impulse, there may not be an associated mechanical contrac-
the presence of wide-­QRS complexes makes type II block more likely. tion. The terms premature atrial contraction and premature ventricu-
Type II second-­degree AV block arises from senescent degenera- lar contraction are widely used but are misleading because contraction
tion, drug toxicity, ischemia, or other pathologic conditions; it gener- may not occur with the extra electrical activity seen on the ECG. The
ally carries a worse prognosis than type I second-­degree AV block. In extrasystole and its preceding impulse are the couplet, and the cou-
acute myocardial infarction, type II second-­degree AV block is associ- pling interval is the period between these two beats. Bigeminy (Fig.
ated with anterior wall injury and is often a precursor to complete AV 65.16) occurs when there is an extrasystole after every native beat so
block. No specific therapy is needed aside from ensuring that pacemak- that every other impulse is extrasystolic; trigeminy (every third beat)
ing capability is immediately available. and quadrigeminy (every fourth beat) are similar. Most extrasystoles
are the result of enhanced automaticity from the atria, AV node, His-­
Third-­Degree Atrioventricular Block Purkinje system, or ventricles.
Third-­degree AV block, also known as complete heart block, is absent
conduction of any atrial impulses (Fig. 65.15). Complete heart block Premature Atrial Contractions
is typically accompanied by a slow escape rhythm, with the width Premature atrial contractions (PACs; Fig. 65.17) are common and usu-
and frequency of QRS complexes depending on the site of the escape ally have little clinical significance. PACs on the ECG are an abnormal

Fig. 65.13  Second-­degree atrioventricular block, type I (Wenckebach). Note the prolongation of the PR inter-
val between the second and third beats, followed by a nonconducted atrial impulse.
BOX 65.5  Causes of Grouped Impulses
Wenckebach mechanism (usually at atrioventricular node, but can occur else-
where)
Sinoatrial exit block
Atrial tachycardia or flutter with alternating conduction
Frequent extrasystoles
Nonconducted atrial trigemini
Concealed or interpolated extrasystoles
P wave early within a cardiac cycle, although sometimes the P wave
may be difficult to detect if it is buried within the preceding T wave.
Most PACs will depolarize the sinus node, resetting its refractory
period. Because of this, the P-­P interval between two sinus beats sur-
rounding a PAC will be less than twice the intrinsic P-­P cycle length
(see Fig. 65.17). If a PAC reaches the AV node or infranodal conducting
system during its absolute refractory period, there will be no ventricu-
lar depolarization. A nonconducted (or blocked) PAC typically results
in a noncompensatory pause (i.e., R-­R interval less than twice the
intrinsic R-­R cycle; Fig. 65.18) because the sinus node is reset. Blocked
PACs are a common cause of electrocardiographic pauses and are eas-
ily overlooked. On occasion, a PAC can be the precipitant of a more
important dysrhythmia, such as atrial fibrillation, atrial flutter, or par-
oxysmal supraventricular tachycardia (PSVT).
If a PAC reaches the infranodal conducting system during its rel-
ative refractory period, the QRS complex is widened (or aberrant),
typically with a right bundle branch block (RBBB) pattern. Because
the refractory period depends on the previous cycle length, an early-­
arriving PAC that follows a long cardiac cycle is more likely to be aber-
rantly conducted. This pattern can happen in atrial fibrillation, creating
wide-­QRS complex impulses that are not ventricular in origin.
PACs are benign and require no specific treatment, but they may
accompany catecholamine excess, myocardial ischemia, heart failure,
hyperthyroidism, or a metabolic abnormality.
Premature Ventricular Contractions
Premature ventricular contractions (PVCs) occur in a wide variety of
states. Occasional PVCs are common in healthy adults or conditions
associated with catecholamine excess, such as pain, anxiety, and use of
stimulants (e.g., caffeine, nicotine, cocaine, amphetamines). Pathologic
conditions associated with frequent PVCs include myocardial infarc-
tion, potassium or magnesium disturbances, and medication toxicity
(notably any with sodium channel-­blocking or sympathetic enhancing
CHAPTER 65  Dysrhythmias 901
activity). Although usually not requiring intervention, frequent PVCs
may herald VT, especially in the setting of acute myocardial infarction
or in patients with a prolonged QT interval.
A PVC appears as a wide-­QRS complex extrasystole without a pre-
ceding P wave (Fig. 65.19). Because retrograde conduction of a PVC
rarely extends far enough to capture and reset the SA node, atrial
impulses continue to arrive at the AV node at the intrinsic sinus rate.
As a result, the R-­R interval surrounding a PVC ends up being equal to
exactly twice the intrinsic R-­R interval length (see Fig. 65.19), a phe-
nomenon termed a compensatory pause. Rarely, a PVC will capture the
SA node, resulting in a noncompensatory pause, or will fail to capture
the AV node, leaving the underlying rhythm completely unaffected
(a so-­called interpolated PVC; Fig. 65.20).
The morphology of a PVC depends on the origin of the impulse,
with a left bundle branch block (LBBB) appearance resulting from an
extrasystolic focus in the right ventricle, and vice versa. Multiform (or
multifocal) PVCs come from more than one source and have vari-
able morphologies. When a PVC occurs at or around the time that a
supraventricular impulse is set to depolarize the ventricle, the result is
a fusion QRS complex (Fig. 65.21). Table 65.4 lists common features of
PACs and PVCs.
Direct therapy for PVCs is focused on correcting any precipitating
condition whether it is catecholamine excess, drug effect, electrolyte
imbalance, or cardiac ischemia (Box 65.6). Often, PVCs do not require
treatment in the ED. When occurring in isolation, symptomatic PVCs
may be treated with a beta blocker (metoprolol, 5 to 10 mg IV or 25
to 50 mg PO), although this is rarely needed. Although IV lidocaine
suppresses PVCs, it should not be used in the absence of VT because of
the risk of asystole with limited clinical benefit.
Narrow-­Complex Tachycardia
Narrow-­complex tachycardias have a QRS complex duration of 0.12
seconds or less on the surface ECG and a ventricular rate of more
than 100 beats//min. The term supraventricular tachycardia may be
confusing; sometimes it is used specifically to note AV reentry tachy-
cardia, but it can denote any tachycardia originating at or above the
AV node.
ECG features that help distinguish between different narrow-­
complex tachycardias include the appearance of P waves and the
regularity or irregularity of the R-­R interval. For example, a narrow-­
QRS complex tachycardia with an irregular R-­R interval and no clear
P waves is almost certainly atrial fibrillation. With rapid tachycar-
dias, evidence of atrial depolarization is often obscured by ventric-
ular repolarization; for example, with a regular, narrow-­complex
902 PART III  Emergency Medicine by System

Mobitz type II second-degree AV block

P P P P P P P P P

B
Fig. 65.14  (A) Second-­degree atrioventricular (AV) block, type II. In this example, 3 : 1 conduction is shown.
(B) Second-­degree AV block with 2 : 1 conduction. From the rhythm strip alone, it is difficult to categorize
this as a type I or II block. (A from Goldberger AL, Goldberger E. Clinical electrocardiography. ed 2. St Louis:
Mosby; 1981.)

6 sec

Fig. 65.15 Complete (third-­degree) atrioventricular block. Note that there is no constant relationship of P
waves to QRS complexes, even though some are noted in close proximity.

Fig. 65.16  Ventricular bigeminy.

 CHAPTER 65  Dysrhythmias 903

Fig. 65.17  Premature atrial contractions.

1220 msec

1240 msec 1360 msec

Fig. 65.18  Premature atrial contractions (PACs) with noncompensatory pauses and one aberrantly conducted
impulse (upper strip). Note that conducted and nonconducted PACs reset the sinus node, with the latter
creating a pause.

A B

Fig. 65.19  Premature ventricular contractions with compensatory pause. Note that a sinus P wave can be
seen in the T wave of the extrasystolic beat. Also, note the secondary T wave changes in beats 1 and 4 (the
T wave is opposite the main deflection of the QRS complex).

tachycardia at a rate of 150 beats/min, it can be challenging to dis-

tinguish sinus tachycardia from atrial flutter or a junctional rhythm.
Vagal maneuvers or adenosine may transiently slow AV nodal con-
duction and expose atrial depolarization to aid diagnosis. Alterna-
tively, the patient may convert to sinus rhythm, in which case an
AV nodal reentrant tachycardia exists. In the post-­heart transplant
patient or anyone with cardiac denervation, adenosine may cause an
II exaggerated response. It should be used carefully and doses of 1.5 to
Fig. 65.20  Interpolated premature ventricular contraction. 3 mg for adults, if not avoided altogether.
904 PART III  Emergency Medicine by System

F F

V4

V4
Fig. 65.21  Sinus rhythm with premature ventricular contraction and run of accelerated idioventricular rhythm.
Note fusion beats (F) displaying a hybrid appearance of both morphologies.

TABLE 65.4  Features Distinguishing BOX 65.6  Causes of Premature Ventricular

Premature Atrial Contractions With Abnormal Contractions and Ventricular Tachycardia
Conduction From Premature Ventricular
Acute or previous myocardial infarction or ischemia
Contractions Hypokalemia
Premature Atrial Premature Ventricular Hypoxemia
Contractions Contractions Ischemic heart disease
Valvular disease
No compensatory pause Fully compensatory pause (unless
Catecholamine excessa
interpolated)
Other drug intoxications (especially cyclic antidepressants)
Preceding P wave (different from No preceding P waves (although
Idiopathic causesb
sinus P wave; occasionally buried retrograde atrial conduction can
Digoxin toxicity
in T wave) cause inverted P wave after QRS)
Hypomagnesemia
Usually classic right bundle branch Left bundle branch block, right bundle Hypercapnia
block pattern (especially if long-­ branch block, or hybrid pattern Class I antidysrhythmic agents
short cycle sequence appears) Ethanol
identical to sinus QRS Myocardial contusion
QRS axis normal or near-­normal Frequently bizarre QRS axis Cardiomyopathy
QRS rarely > 0.14 s QRS often > 0.14 s Acidosis
Alkalosis
Methylxanthine toxicity
a Relative increase in sympathetic tone from drugs (direct or indirect)
Sinus Tachycardia or conditions that augment catecholamine release or decrease
Sinus tachycardia displays a regular, usually narrow-­complex tachycar- parasympathetic tone.
dia, with normal P waves preceding each QRS complex (Fig. 65.22) b Isolated premature ventricular contractions (PVCs) can occur in up to

on the ECG. In adults, sinus tachycardia rarely exceeds a rate of 170
beats/min; in infants and young children, it is not unusual to see rates
above 200 to 225 beats/min. Sinus tachycardia tends to speed up or
slow down in a graded and continuous manner over time, relayed by
history or observed under care.
Sinus tachycardia is often a response to physiologic stress or a com-
pensation to increase cardiac output in the setting of a relative lack of
perfusion or oxygen delivery. Usually, the effect is beneficial, as seen
with hypovolemia, anemia, or hypoxemia; efforts to slow the heart rate
compensation without addressing the underlying pathophysiology are
likely to exacerbate the situation. Occasionally, sinus tachycardia is
counterproductive, as in acute decompensated heart failure or aortic
stenosis, in which a decrease in filling time further compromises car-
diac output. Even in these settings, therapy is aimed first at the under-
lying problem rather than the tachycardia.
50% of young subjects without obvious cardiac or noncardiac disease;
however, multiform and repetitive PVCs and ventricular tachycardia are
rarely seen in this population.
Sinus tachycardia can be seen with any sympathetic excess, whether
endogenous (e.g., pain, anxiety, fever, hyperthyroidism) or exogenous
(e.g., stimulants, other drugs). The approach to the patient with sinus
tachycardia centers on identifying and addressing the cause(s). Beta
blockers are rarely used to treat sinus tachycardia.
Atrial Tachycardia
Atrial tachycardia (AT) is an atrial rhythm with more than 100 QRS
complexes/min arising from a nonsinus node atrial site(s). An ECG
will be notable for abnormal P waves, all or mostly related to each QRS
complex (Fig. 65.23). If the site of origin is close to the sinus node,
 CHAPTER 65  Dysrhythmias 905

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V1

II

V5
Fig. 65.22  Sinus tachycardia.

I R

II L

III F

Fig. 65.23 Atrial tachycardia (with 2 : 1 conduction) in a patient with digoxin toxicity. (From Marriott HJL,
Conover MB. Advanced concepts in dysrhythmias. ed 2. St. Louis: Mosby; 1989.)

atrial depolarization waves may look like a normal P wave. Depending
on the atrial rate, the AV conduction ratio may be 1:1, 2:1, or higher.
AT is common in children and young adults with structural heart
disease, often precipitated by the occurrence of a PAC. The rhythm is
usually transient and does not require specific therapy. AT can also
occur in patients with hypoxemia, metabolic disturbances, or drug tox-
icity. In patients taking digoxin, suspect toxicity with AT, particularly
in the presence of 2:1 or higher-­grade AV block.
Multifocal AT (MAT) is a form of AT with three or more distinct
P wave morphologies, and varying PR and P-­P intervals from the
multiple ectopic atrial foci (Fig. 65.24). MAT is associated with pul-
monary disease (usually chronic obstructive pulmonary disease) in
up to 60% of cases but can also be seen in the presence of primary
cardiac pathology. On the surface ECG, MAT is often mistaken for
atrial fibrillation because of the nonuniform atrial activity and irreg-
ular R-­R intervals.
The approach to patients with AT is to identify and treat any pre-
cipitating factors, such as hypoxia or hypoxemia, electrolyte abnormal-
ities, or drug toxicity. In patients with suspected hypomagnesemia, give
supplemental magnesium (2 g IV over 5 minutes). Vagal maneuvers
and adenosine are unlikely to be effective in AT or MAT, although
these may help unmask the atrial activity. Pharmacologic therapy to
slow AV conduction with a beta blocker or calcium channel blocker
aids in the symptomatic but stable patient. Because AT and MAT are
906 PART III  Emergency Medicine by System
Fig. 65.24  Multifocal atrial tachycardia. Note that although the rhythm is irregular, at least three distinct P
wave morphologies are present.
Fig. 65.25  Atrial fibrillation with rapid ventricular response. Note that the irregularity could be easily over-
looked.
often precipitated by underlying illnesses, electrical cardioversion often
fails or the rhythm recurs.
Atrial Fibrillation
Atrial fibrillation is electrical supranodal chaos; it starts from unpat-
terned depolarization of atrial tissues caused by multiple microreen-
try circuits, generating 300 to 600 atrial impulses/min. This chaotic
activity reduces cardiac output due to both a loss of coordinated atrial
contractions and a rapid ventricular rate, both of which may limit the
diastolic filling and stroke volume of the ventricles.
Atrial fibrillation is the most common sustained dysrhythmia,
increasing with age; it affects 1% of the population older than 60 years
and 5% of those 69 years old or more. Patients with atrial fibrillation
can develop left atrial thrombi, especially in the left atrial appendage,
with consequent embolic events. The risk of stroke is three to five times
greater than in those without atrial fibrillation. Appendageal occlusion
through transcatheter approaches may alter the need for long-­term,
clot-­directed therapy to mitigate embolic risks. Also, ablation therapies
may restore sinus rhythm without the need for ongoing drug therapy.
Atrial fibrillation may be paroxysmal (spontaneously converts),
persistent (requires cardioversion to convert), or permanent (when
no further efforts to restore sinus rhythm are planned). Long-­term
approaches to management depend on many factors, including
chronicity, symptomatology, underlying heart disease, and other
comorbidities.
The electrocardiographic hallmark of atrial fibrillation is an irreg-
ularly irregular QRS pattern (Fig. 65.25). Although atrial fibrillation
is not the sole cause of an irregular ventricular rhythm, it is the most
BOX 65.7  Causes of Completely Irregular
(Chaotic) Rhythms
Atrial fibrillation
Atrial tachycardia or flutter with varying conduction
Multifocal atrial tachycardia
Multiple extrasystoles
Wandering pacemaker (usually atrial)
Parasystole
common (Box 65.7). Atrial fibrillatory waves appear coarse or fine
based on their amplitude and are often best appreciated in the inferior
leads or lead V1.
Typically, the ventricular rate in adults with atrial fibrillation does
not exceed 150 to 170 beats/min and often is slower, particularly in
the presence of nodal blocking agents. Atrial fibrillation in an adult
with a ventricular rate exceeding 200 beats/min strongly suggests
the presence of an accessory conduction pathway and has import-
ant implications for management (see later). Frequently, rapid atrial
fibrillation with an accessory path will have a wide-­QRS complex,
but not always; if the irregularity of ventricular depolarization is not
sought by the careful use of a caliper or similar measurement, it is
easy to mistake this wide but chaotic rhythm for VT. When a wide-­
QRS complex is seen at rates below 200 beats/min but with ventric-
ular chaos, an existing or acquired bundle branch block with atrial
fibrillation is likely present.

MCL1
Fig. 65.26 Atrial fibrillation with classic Ashman phenomenon series of beats. Note the long-­short cycle
before aberrantly conducted impulses are sustained for four beats. (From Marriott HJL, Conover MB.
Advanced concepts in dysrhythmias. ed 2. St. Louis: Mosby; 1989.)
BOX 65.8  Causes of Atrial Fibrillation
Hypertensive heart disease
Cardiomyopathy
Ischemic heart disease
Valvular disease (especially mitral)
Congestive heart failure
Pericarditis
Hyperthyroidism
Sick sinus syndrome
Myocardial contusion
Acute ethanol intoxication (holiday heart syndrome)
Idiopathic
Cardiac surgery
Catecholamine excess
Pulmonary embolism
Accessory pathway (Wolff-­Parkinson-­White) syndrome
The Ashman phenomenon refers to aberrant ventricular conduc-
tion of an early-­arriving atrial impulse following a relatively long R-­R
interval, the result of a partially refractory His bundle. Such aberrantly
conducted impulses are commonly seen in atrial fibrillation but can
occur in any irregular rhythm in which long-­short cycle sequences
occur; they typically assume an RBBB pattern (Fig. 65.26). Ashman
beats can be mistaken for PVCs or runs of VT if sustained.
Atrial fibrillation is usually associated with underlying heart dis-
ease. The most common etiology is hypertension, but it can also occur
with ischemic or valvular disease (Box 65.8). Atrial fibrillation may
occur in isolation (lone atrial fibrillation) or as a manifestation of sys-
temic conditions such as hyperthyroidism. As many as one-­third of
patients with congestive heart failure also have atrial fibrillation.
The presentation of patients with atrial fibrillation is variable.3,4 For
example, patients without underlying cardiopulmonary disease may
tolerate atrial fibrillation with ventricular rates up to 150 beats/min,
noting only palpitations or exercise intolerance. Conversely, a patient
with left ventricular dysfunction and new atrial fibrillation may expe-
rience dyspnea at rest. In a patient with preexisting atrial fibrillation
who presents with a rapid ventricular rate, the initial evaluation should
determine if the tachycardia is a response to some other hemodynamic
stress, such as decompensated heart failure, sepsis, hypovolemia, mas-
sive pulmonary embolism, or cardiac tamponade. Identifying acute
CHAPTER 65  Dysrhythmias 907
underlying conditions may direct timely interventions.5 Failure to rec-
ognize the underlying cause of tachycardia may result in counterpro-
ductive attempts at rate control or cardioversion.
For stable patients with rapid atrial fibrillation, administration
of an AV nodal blocking agent to achieve a target ventricular rate of
120 beats/min or less is the first step.3,4 IV calcium channel blockers
(e.g., diltiazem, verapamil) or beta blockers (e.g., metoprolol) are eas-
ily titrated and can be followed by an oral agent. Nodal agents should
not be used for rate control in the setting of anterograde (wider QRS)
accessory pathway conduction because AV conduction may be pre-
venting the ventricular rate from accelerating and degenerating into
ventricular fibrillation.
The debate over rhythm or rate control for patients with established
atrial fibrillation is ongoing without a definitive answer for all patient
populations. Among patients with heart failure, a rhythm control strat-
egy via catheter ablation (but not with antidysrhythmic drugs) is asso-
ciated with improvement in clinical outcomes.
In choosing rate control for the long term, the ideal target is
unclear, with some advocating for a resting rate of 80 beats/min or less
(American Heart Association (AHA) class IIa recommendation) while
acknowledging that for patients with preserved left ventricular func-
tion, a lenient rate-­control strategy of <110 bpm may be reasonable as
long as patients remain asymptomatic.3
If atrial fibrillation has been present longer than 2 days in the
absence of therapeutic anticoagulation, cardioversion may increase the
risk of systemic embolization from preexisting atrial thrombus. How-
ever, for patients with new-­onset or newly recurrent atrial fibrillation
(i.e, duration of 48 hours or less) or for those already on therapeutic
anticoagulation, ED cardioversion is safe. Cardioversion can also be
performed following transesophageal echocardiography demonstrat-
ing the absence of atrial thrombus.
The choice of electrical versus pharmacologic cardioversion
depends on institutional factors and patient preference, but success
rates are generally higher with electrical conversion.3,4,6 A strategy of
procainamide therapy first, followed by electrical cardioversion for
patients not converted pharmacologically within 30 minutes, is another
option that obviates the need for electrical cardioversion in about half
of patients.7 In patients with new or recurrent atrial fibrillation of less
than 48 to 72 hours duration, up to 50% will convert spontaneously to
sinus rhythm within 24 hours.
Various agents are available for the pharmacologic cardioversion
of patients with stable atrial fibrillation in the ED, including the class
908 PART III  Emergency Medicine by System

BOX 65.9  Pharmacologic Approach to Atrial BOX 65.10  CHA2DS2VASC Scoring for Guiding
Fibrillation and Flutter Conversion Clot-­Directed Therapy in Atrial Fibrillation
IV procainamide, 30–50 mg/min, up to a total dose of 18–20 mg/kg (12 mg/kg in
patients with congestive heart failure) or until conversion or side effects occur Clinical Feature Points
or Congestive heart failure 1
Amiodarone, 150 mg IV over 10{en dash}15 minutes, followed by 1 mcg/min Hypertension 1
IV infusion for 6 hours then 0.5 mcg/min IV for 18 hours (or switch to oral) Age ≥ 75 yr 2
or Diabetes mellitus 1
Ibutilide, 0.015–0.02 mg/kg IV, over 10–15 min (conversion usually occurs Any previous stroke, transient ischemic attack, embolism 2
within 20 min if successful) Gender—female 1
or Age, 65–74 yr 1
Oral propafenone, 600 mg (contraindicated in the setting of structural heart Vascular disease (history of MI, PAD, or aortic atherosclerosis) 1
disease or ischemia)
or Vascular disease—myocardial infarction, peripheral vascular disease, aortic
Oral flecainide, 300 mg (contraindicated in the setting of structural heart plaque
disease or ischemia) Actions:
Note: If needed, a calcium channel blocker can be given before the type IA • Score 0— no anticoagulant therapy
agent (if no contraindications are present) to lower the ventricular response • Score 1—oral anticoagulation should be considered
rate to below 120 beats/min and to attenuate further tachycardia from the • Score 2 or higher—oral anticoagulation is recommended
vagolytic effects of these agents.

BOX 65.11  HAS-­BLED Scoring System to

IA, IC, and III antidysrhythmics (Box 65.9). In practice, ibutilide,
amiodarone, and procainamide are most commonly used in the ED
setting. Of these agents, ibutilide is associated with the highest rates
of conversion to sinus rhythm, but, like all class IC antidysrhythmics,
is best avoided in patients with structural or ischemic heart disease.
Amiodarone is safe in this population and has the additional advan-
tage of slowing the ventricular response. Procainamide is a first-­line
agent in patients with a suspected accessory pathway (very fast ven-
tricular responses or known presence) because it does not impact AV
conduction.
Rarely, rapid rates or irregularity make synchronized cardiover-
sion efforts impossible; in this setting, it is appropriate to proceed with
unsynchronized cardioversion while being prepared to re-­shock if ven-
tricular dysthymia ensues.8,9 Following electrical cardioversion, there
is an increased risk of thromboembolism in the initial 30 days.
Although long-­term antiplatelet or anticoagulation therapy typi-
cally falls beyond the scope of the ED, starting early can enhance help
avoid embolism and enhance patient compliance. The AHA and Euro-
pean Society of Cardiology recommend using the CHA2DS2-­VASc
score to guide anticoagulation therapy in those with atrial fibrillation
(Box 65.10).3,4 Anticoagulation reduces the overall risk of stroke by
almost 70 percent, but with an increased risk of major bleeding; there-
fore, the risk-­to-­benefit ratio of any anticoagulation strategy must be
assessed for patients at higher risk for bleeding (Box 65.11). The choice
of coagulation therapy may be influenced by many institutional and
patient-­specific factors, but the direct oral anticoagulants (DOACs),
including apixaban, dabigatran, edoxaban, or rivaroxaban, have an
overall safety profile that is superior to warfarin10,11.
Atrial fibrillation alone is not an indication for hospital admission.
Observation or admission are appropriate for atrial fibrillation com-
plicated by other conditions, accompanied by acute or exacerbated
cardiopulmonary disease, when duration is unknown and follow-­up
uncertain, and for symptomatic patients who fail cardioversion. Abla-
tion therapy is another option after new-­onset or recurrent episodes.12
Atrial Flutter
Atrial flutter has ECG features of atrial depolarization occurring
at a regular rate of 250 to 350 beats/min (300 beats/min is classic)
Assess 1-­Year Risk of Major Bleeding in Patients
Taking Anticoagulants with Atrial Fibrillation
Condition Points
H Hypertension: (uncontrolled, >160 mmHg systolic) 1
A  Abnormal renal function: Dialysis, transplant, Cr 1
>2.26 mg/dL or >200 μmol/L 1
Abnormal liver function: Cirrhosis or Bilirubin >2×
Normal or AST/ALT/AP >3× Normal
S  Stroke: Prior history of stroke 1
B  Bleeding: Prior Major Bleeding or Predisposition to 1
Bleeding
L  Labile INR: (Unstable/high INR), Time in Therapeutic 1
Range < 60%
E  Elderly: Age > 65 years 1
D  Prior Alcohol or Drug Usage History (≥8 drinks/week) 1
Medication Usage Predisposing to Bleeding: 1
(Antiplatelet agents, NSAIDs)
A score of ≥3 indicates “high risk” and indicates the need for caution
caused by an atrial reentry mechanism (Fig. 65.27). Flutter waves
on the ECG are broad, sawtooth-­appearing, regular depolarizations
prior to QRS complexes, with the latter occurring at some fraction
of the atrial rate. The ventricular rate in atrial flutter is often rapid,
but in the absence of a bypass tract (in which 1 : 1 conduction is
possible), the conduction ratio is limited by the refractory period
of the AV node. With 2 : 1 conduction, the classic ventricular rate
is 150 beats/min, often making flutter waves difficult to appreci-
ate and allowing the rhythm to be mistaken for sinus tachycardia.
Because the atrial rate can vary, the ventricular rate range widely
varies also. When the conduction ratio changes from beat to beat,
this is termed atrial flutter with variable conduction, with a resul-
tant irregular ventricular rate. This can be distinguished from atrial
fibrillation by looking for a pattern of atrial depolarization rather
than chaotic atrial activity.

Atrial flutter often accompanies pulmonary disease, structural
heart disease, particularly valvular heart disease, and cardiomyopa-
thies. The acute management of atrial flutter parallels that of atrial
fibrillation with a few special considerations. Because AV conduc-
tion occurs at fixed ratios in atrial flutter, the administration of beta
blocker or calcium channel blocker therapy can result in an abrupt
rate change, making it more challenging to titrate therapy to a desired
target rate.
Atrial flutter is more sensitive to DC cardioversion (up to 90% con-
version rate) than atrial fibrillation and usually requires lower energy
(20 to 50 J) for conversion to sinus rhythm. Atrial flutter is more resis-
tant to chemical cardioversion (<50% success) than new-­onset, non-­
valvular atrial fibrillation. In most other respects, ED patients with
atrial flutter are managed similarly to those with atrial fibrillation; in
particular, anticoagulation therapy at discharge should be considered
similarly to atrial fibrillation.
Atrioventricular Nodal Reentrant Tachycardia
Also known by the less precise term PSVT, or just SVT), AVNRT is a
regular, narrow-­complex rhythm with a ventricular rate of 130 beats/
min or greater, commonly more than 160 beats/min (Fig. 65.28).
Lead VI
Leads I and II
B
CHAPTER 65  Dysrhythmias 909
It is the most common nonsinus tachydysrhythmia in young adults.
AVNRT is the result of a reentry circuit within the AV node, with nor-
mal conduction (narrow QRS) down the bundles of His and with ret-
rograde conduction (inverted P waves typically buried within the QRS)
up into the atria (Fig. 65.29).
The onset and spontaneous end of AVNRT is typically abrupt, and
it frequently arises in the context of strenuous exercise or emotional
stress. Most patients with AVNRT are symptomatic, but hemodynamic
instability is unusual in the absence of underlying cardiopulmonary
disease.
If vagal maneuvers fail to restore sinus rhythm, first-­line therapy for
AVNRT is adenosine (6 mg rapid, large-­bore IV bolus followed by a
flush; repeat with 12 mg if no effect on rate). This approach is success-
ful in 85% to 90% of cases and is safe. In refractory cases, diltiazem,
esmolol, or metoprolol are options. Rarely needed, synchronized car-
dioversion (at 100 to 200 J, biphasic preferred) can terminate AVNRT
refractory to pharmacologic therapy or in a patient with hemodynamic
instability.
No specific laboratory testing is needed, although mild troponin
level elevations occur but are of uncertain significance aside from con-
cerns for myocardial ischemia. Most patients can be discharged after
910 PART III  Emergency Medicine by System

Lead III

Lead II

C
Fig. 65.27 (A) Atrial flutter with 2 : 1 conduction and isolated premature ventricular contraction. (B) Atrial
flutter with 2 : 1 conduction. Lead II helps identify characteristic flutter waves. (C) Atrial flutter with 1 : 1
conduction. This is rare and can be mistaken for ventricular tachycardia (lead II).

EC - 48

Fig. 65.28  Paroxysmal supraventricular tachycardia. Note the narrow, regular QRS complexes.

terminating AVNRT with adenosine or vagal maneuvers and typi-
cally require no testing beyond an ECG, including in the field setting.
Patients with frequent recurrences are candidates for prophylaxis with
a beta blocker or calcium channel blocker or ablation therapy. Starting
prophylactic therapy from the ED is appropriate for those patients with
an established plan for follow-­up.
Junctional Tachycardia
In contrast to the bursts seen in AVNRT, JT show sustained ventricular
rates but rarely exceeds 130 beats/min. JT is associated with structural
heart disease, metabolic disturbances, or drug toxicity. Treatment
should address underlying conditions, although a trial of nodal block-
ade with calcium channel blockers or beta blockers is an option if the
rate seems to be deleterious.
Preexcitation and Accessory Pathway Syndromes
The term preexcitation is depolarization of the ventricular myocardium
via an accessory pathway (or bypass tract) linking the atria to the ven-
tricles, circumventing the normal AV node. Accessory pathways do
not have the natural rate limits of the AV node, lending themselves

Circus movement using
AV nodal reentry accessory pathway SA reentry
56% 100% 86%
36% 14%
4%
4%
Fig. 65.29  Location of P waves in common causes of regular narrow-­
complex tachycardia. AV, Atrioventricular; SA, sinoatrial. (From Marriott
HJL, Conover MB. Advanced concepts in dysrhythmias. ed 2. St. Louis:
Mosby, 1989.)
to reentry tachycardia and rapid ventricular rates. Wolff-­Parkinson-­
White (WPW) syndrome is the classic accessory pathway syndrome,
characterized by paroxysmal tachycardia and three resting electrocar-
diographic features (Fig. 65.30):
• Short PR interval (<0.12 second)
• QRS duration longer than 0.10 second
• Slurred upstroke to the QRS complex, referred to as a delta wave
Not all patients with WPW or other preexcitation syndromes
have all the classic features on their surface ECG. Conversely, some
patients with WPW-­like patterns on their resting ECG never develop
reentry tachycardia. Although some with WPW syndrome have
structural disease, most patients have no other underlying cardiac
abnormality (Box 65.12). Atrial fibrillation is seen in up to 30% of
patients with WPW.
The presence of an accessory pathway can form a reentry circuit
together with an AV nodal pathway to produce and sustain a rapid
ventricular rate (Fig. 65.31). When the AV node is being used for
anterograde conduction to the ventricles, and the accessory path
is used for retrograde conduction, it is called an orthodromic AV
reciprocating tachycardia. The QRS complex is typically narrow,
and the ventricular rate is constrained by the refractory period of
the AV node. Conversely, when the accessory pathway is the antero-
grade limb and the AV node is the retrograde limb of the reentry
circuit, it is called an antidromic AV reciprocating tachycardia. In
this scenario, the QRS complex is wide and ventricular rates can be
extremely rapid.
Orthodromic AV reciprocating tachycardia is the most common
presenting dysrhythmia in WPW syndrome and is indistinguishable
clinically from AVNRT. Like AVNRT, orthodromic AV reciprocating
CHAPTER 65  Dysrhythmias 911
tachycardia is treated with vagal maneuvers and adenosine as first-­line
therapies, followed by calcium channel blockers and beta blockers as
second-­line agents.
In contrast, antidromic AV reciprocating tachycardia has charac-
teristic wide-­QRS complexes and may have ventricular rates of 200
beats/min or more and clinical instability. When the typical QRS
antidromic changes are coupled with tachycardia, AV nodal blocking
agents may trigger degeneration into ventricular fibrillation. Simi-
larly, in patients with a very rapid (>220/min) irregular tachycardia
accompanied by a wide-­complex QRS, nodal blockade may risk rapid
deterioration to ventricular fibrillation from unbridled conduction
down the accessory pathway. Procainamide is first-­line therapy for
tachycardia when wide-­QRS complexes suggest conduction down an
accessory pathway; amiodarone is an alternative. Use prompt syn-
chronized electrical cardioversion (100 to 200 J) if there is any clinical
deterioration, failure of pharmacologic therapy, or extreme tachycar-
dia (>250 beats/min).
The Lown-­Ganong-­L evine syndrome is an uncommon acces-
sory pathway syndrome associated with paroxysmal narrow-­
complex tachycardia, short PR interval, and normal QRS complex
without a delta wave. The treatment parallels that for the WPW
syndrome.
Refer all patients with a new or symptomatic accessory pathway for
advanced electrophysiologic care, including pathway identification and
ablation.
Wide-­Complex Tachycardia
Wide-­complex tachycardia refers to any tachydysrhythmia accompa-
nied by a QRS duration of 0.12 seconds or more. Wide-­complex tachy-
cardia can start in the ventricles (i.e., VT) or can originate from above
the AV node but be accompanied by aberrant AV conduction. The
aberrant conduction is caused by an accessory pathway or a bundle
branch block. The presence of AV dissociation or fusion beats on the
12-­lead ECG clearly points to VT; older age and a prior history of myo-
cardial infarction make VT more likely than a supraventricular tachy-
cardia with aberrancy. On the other hand, an irregular tachycardia with
a wide QRS approximating a bundle branch morphology is most likely
atrial fibrillation with aberrant conduction. Although new-­onset VT
patients are usually unstable, the presence of hemodynamic stability
does not exclude VT.
It can be difficult to make the distinction between VT and an SVT
with abnormal conduction when confronted with a wide-­complex
tachycardia in a patient. Many of the decision rules rely on an abil-
ity to discern subtleties of the QRS morphology, and none has per-
fect discriminatory power. (Table 65.5; Fig. 65.32) As a general rule,
consider any new wide-­complex tachycardia to be VT until proven
otherwise.
The classic Wellens criteria are time-­honored but hard to use cri-
teria because of their complexity and lack of order or weighting of
findings. The Brugada ECG criteria describe four features of VT from
among those described in the original Wellens criteria, any one of
which makes the diagnosis of VT. The rhythm needs to be regular for
these to be used because irregularity suggests atrial fibrillation with
altered conduction. The sequential criteria are as follows (Fig. 65.33,
see also Fig. 65.32):
1. Absence of any RS complexes in the precordial leads
2. RS duration (measured from beginning of R to deepest part of S
wave) greater than 100 msec
3. AV dissociation (often present but overlooked; may be best appreci-
ated in inferior limb leads and V1-2; Fig. 65.34)
4. Specific VT morphologic criteria (see Fig. 65.33)
912 PART III  Emergency Medicine by System

I
V2

II

V3
III

162
VR

V4

VL
160

V5

VF

168

170 V6

V1

V2 cont.

B 330 msec

Fig. 65.30  (A) Wolff–Parkinson–White (WPW) syndrome. (B) WPW syndrome with atrial fibrillation. Note the
short refractory period (330 ms). (A from Watanabe Y, Dreifus LS. Cardiac dysrhythmias. New York: Grune
& Stratton; 1977.)
 CHAPTER 65  Dysrhythmias 913

Only the absence of all the Brugada criteria allows the diagnosis assessment or agree on the findings. In patients receiving class I agents,
of SVT. Although the original investigators found excellent sensitivity the Brugada criteria are less reliable.
(98.7%) and specificity (96.5%) in detecting VT, follow-­up investiga- The Griffith criteria use a three-­step approach to identify aber-
tions have shown a lower level of accuracy in ED patients (sensitivity of rancy, first through classic RBBB or LBBB morphologies in V1 and V6
92% to 94%). Often, emergency clinicians are not able to complete the to identify an SVT and then seeking AV dissociation in the remainder
to identify VT (see Figs. 65.32 and 65.34). This approach has a sensi-
tivity of 92% with a lower specificity than that seen with the Brugada
approach. There are no direct, in-­practice comparative data between
BOX 65.12  Diseases Associated With Wolff-­ these two approaches. Finally, the Vereckei criteria (Fig. 65.35)
Parkinson-­White Syndrome examine lead aVR to differentiate between VT and SVT; however, in
practice, these have not been shown to be more effective or accurate,
Idiopathica
limiting their use.
Cardiomyopathy (especially hypertrophic)
Unstable patients with a wide-­complex tachycardia should undergo
Transposition of great vessels
electrical cardioversion (100 J, synchronized and biphasic, if possible).
Endocardial fibroelastosis
For borderline patients, electrical cardioversion with systemic seda-
Mitral valve prolapse
tion or analgesia or pharmacologic treatment with procainamide or
Tricuspid atresia
amiodarone are options.
Ebstein disease
Adenosine is an option after a careful search of the ECG does
a Most common. not suggest VT. Adenosine is should be avoided in suspected VT

Normal AV WPW complex WPW tachycardia WPW tachycardia

WPW with
conduction (preexcitation) (common variety) (uncommon variety)
atrial flutter
fibrillation
Fig. 65.31 Wolff–Parkinson–White (WPW) paths and associated rhythms. AV, Atrioventricular. (A from
Watanabe Y, Dreifus LS. Cardiac dysrhythmias. New York: Grune & Stratton; 1977.)

TABLE 65.5  Features Distinguishing Ventricular Tachycardia From Supraventricular

Tachycardia With Abnormal Conduction
Parameter
Clinical features
Physical examination
Electrocardiogram
Specific QRS patterns
Supraventricular Tachycardia Plus
Ventricular Tachycardia Aberrancy
Age ≥ 50 yr Age ≤ 35 yr
History of myocardial infarction, congestive heart failure, CABG, or ASHD None
Previous history of ventricular tachycardia Previous history of supraventricular tachycardia
Cannon A waves Absent
Variation in arterial pulse Absence of variability
Variable first heart sound Absence of variability
Fusion beats None
AV dissociation Preceding P waves with QRS complexes
QRS >0.14 s QRS usually <0.14 s
Extreme left axis deviation (30 degrees) Axis normal or near-­normal
No response to vagal maneuvers Slow or terminate with vagal maneuvers
V1: R, qR, or RS V1: rSR′
V6: S, rS, or qR V6: qRs
Identical to previous ventricular tachycardia tracinga Identical to previous supraventricular tachycardia
Concordance of positivity or negativityb tracinga

ASHD, Arteriosclerotic heart disease; AV, atrioventricular; CABG, coronary artery bypass graft; LAD, left anterior descending.
aIf proven by electrophysiologic studies or by a preponderance of evidence.
bMain deflection of QRS complex either positive or negative in every precordial lead.
914 PART III  Emergency Medicine by System

Absence of an RS complex in all precordial leads? BBB pattern

Right
V1 rSR′ pattern with R ′> rRS (RS) pattern with
Yes No
R > S; Q wave
V6 <40 msec and <2 mm (0.2 mV) were allowed
Left
VT Next question V1 rS or QS pattern with time to 5 wave
nadir <70 msec
V6 R wave with no Q wave
R to S interval >100 ms in one precordial lead?
BBB = bundle branch block.
If no classic BBB pattern as noted above that would define SVT with
Yes No aberrancy, search for AV dissociation; if present, VT is diagnosed
and if absent, SVT is diagnosed by default.

B
VT Next question

Atrioventricular dissociation?

Yes No

VT Next question

Morphology criteria for VT present

both in precordial leads V1–2 and V6?

Yes No

VT SVT with aberrant conduction

A
Fig. 65.32  (A) Brugada four-­step approach for differentiating ventricular tachycardia (VT) and wide-­QRS supraven-
tricular tachycardia. Only when the response to all four questions is negative is a supraventricular rhythm with
abnormal conduction diagnosed. As soon as a single “yes” answer is noted, VT is diagnosed. (B) Griffith approach,
in which aberrant conduction is sought in leads V1 and V6 (right bundle branch block [RBBB] or left bundle branch
block [LBBB], classic appearances), followed by a search for atrioventricular (AV) dissociation. If classic RBBB and
LBBB patterns are absent, or if the remainder of the leads have AV dissociation, VT is diagnosed. ([A] From Bru-
gada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide
QRS complex. Circulation. 1991;83:1649–1659; [B] adapted from Griffith MJ, Garratt CJ, Mounsey P, Camm AJ.
Ventricular tachycardia as default diagnosis in broad complex tachycardia. Lancet. 1994;343:386–388.)

LEAD V1 LEAD V6
Monophasic R R to S
ratio < 1
QR QS
RS QR
A B
Fig. 65.33  Morphology associated with the fourth criterion in the Brugada system. (A) In patients with a right
bundle branch-­appearing complex. (B) In patients with a left bundle branch-­appearing complex.
or if there is an irregular or very rapid ventricular rate (≥250 beats/
min). It should be used with caution after heart transplantation.
Most SVTs will slow or terminate with adenosine, and only rare VT
forms respond; any ill effects of adenosine are usually fleeting. Other
pharmacologic therapies for stable VT are discussed later. If phar-
macologic treatment fails, synchronized cardioversion should be
performed.
Ventricular Tachycardia
VT originates within or below the His bundle. Nonsustained VT refers
to short episodes (<30 seconds) reverting spontaneously, whereas sus-
tained VT is prolonged. Reentry mechanisms are the most common
cause of VT, although automatic and triggered mechanisms occur.
Most patients with VT have underlying heart disease, especially isch-
emic and nonischemic cardiomyopathy.
Monomorphic ventricular tachycardia is the most common form
of VT and is characterized by morphologically consistent QRS com-
plexes, usually in a regular pattern at a rate of 150 to 200 beats/min
(Fig. 65.36). Polymorphic ventricular tachycardia is seen with vary-
ing QRS morphologies and suggests a more severe underlying disease
(Figs. 65.37 and 65.38).
For stable patients with VT, amiodarone (3 to 5 mg/kg IV over 20
minutes, often 250 to 350 mg) is the first-­line agent, with reported suc-
cessful termination of up to 90%. Procainamide (30 to 50 mg/min IV,
up to a total of 18 mg/kg or until VT is terminated) is a second-­line
agent. Lidocaine (1.0 to 1.5 mg/kg IV bolus, up to 3 mg/kg maximum,
followed by an infusion) is an alternative to amiodarone with similar
success rates in some studies. Unstable patients or those with VT refrac-
tory to pharmacotherapy should undergo synchronized cardioversion
CHAPTER 65  Dysrhythmias 915
LEAD V1 or V2 LEAD V6
R > 0.03 second
QR
> 0.07 second
to nadir of S
QS
Notched or
slurred S
with 100 J (biphasic preferred); escalating doses of up to 200 J biphasic
or 360 J monophasic are occasionally needed.
Cardiology should be consulted for patients with VT. Ablation ther-
apy, along with medical optimization, may aid long-­term management.
Torsades de Pointes
Torsades de pointes is translated as “twisting of the points” and is a
paroxysmal form of polymorphic VT that meets the following clinical
criteria (see Fig. 65.38):
1. Ventricular rate greater than 200 beats/min
2. Undulating QRS axis, with the polarity of the complexes appearing
to shift about the baseline
3. Paroxysms of less than 90 seconds
Torsades de pointes occurs in the setting of a prolonged QT inter-
val, a reflection of abnormal ventricular repolarization. A prolonged
QT interval can be congenital or acquired. Women are at a greater risk
for torsades de pointes. Acquired torsades de pointes is much more
common than congenital and is pause-­dependent, triggered by a slow
heart rate.
Acquired QT prolongation is the most common form seen outside a
specialized pediatric setting and usually has multifactorial causes (Box
65.13). Common triggers include electrolyte disturbances (e.g., hypo-
kalemia, hypomagnesemia) or many different medications (notably
class IA and IC agents but also many others; see Box 65.13), especially
when used in combination.
Treatment of torsades de pointes in stable adult patients involves
correcting any underlying metabolic or electrolyte abnormalities and
increasing the heart rate to shorten ventricular repolarization. Class IA
and IC antidysrhythmics should not be used in patients with torsades
916 PART III  Emergency Medicine by System

II

P P P P P P P P

V1

V5
A

II

P P P P P P P P

V1

V5
B

II

P P P P P P P P P P

V1

V5
C
Fig. 65.34 (A, B) Ventricular tachycardia. Note atrioventricular dissociation. (C) Intermittent, nonsustained
ventricular tachycardia. Atrioventricular dissociation is evident. (Courtesy Dr. Edward Curtis.)
 CHAPTER 65  Dysrhythmias 917

Yes
Is there an initial R wave in lead aVR? Diagnose VT

No

Is there an initial R or Q wave in aVR Yes

Diagnose VT
that is >40 msec?

No

Is there a negative directed notch and Yes

Diagnose VT
a mostly negative QRS in aVR?
No

Is the initial aVR ventricular activation Yes

velocity (vi) divided by the terminal Diagnose VT
velocity (v2) 17 or less?

No

Diagnose SVT
Fig. 65.35  Vereckei criteria for differentiation of ventricular tachycardia (VT) from supraventricular tachycardia
(SVT).

de pointes. Empirical IV magnesium sulfate (1 to 2 g quickly) effec-
tively treats torsades de pointes, even in the absence of hypomagnese-
mia, and may prevent recurrence if electrical cardioversion succeeds.
A baseline ventricular rate of 100 to 120 beats/min is usually enough
to prevent acquired torsades de pointes, achieved by overdrive pacing
(i.e., external pacing at a rate greater than the patient’s intrinsic rate) or
via β-­adrenergic (isoproterenol) infusion. Unstable patients or those
with sustained torsades de pointes should undergo electrical cardiover-
sion, recognizing that synchronization may not be possible.
Congenital torsades de pointes is rare and triggered by sympathetic
excess or tachycardia; it is usually seen in children and young adults.
Patients often have syncope during exertion and a prolonged QT inter-
val on the ECG. In contrast to acquired forms, congenital torsades de
pointes is treated with beta blockers.
Brugada Syndrome
Brugada syndrome is a ventricular dysrhythmia triggering syncope or
sudden cardiac death in the absence of structural heart disease. This
syndrome links to an inherited disorder of sodium channels and is
commonly diagnosed in men during young adulthood. The Brugada
electrocardiographic pattern shows a downward coved or humped
(saddleback) ST segment elevation in leads V1 to V3 (Fig. 65.39),
sometimes simulating an RBBB appearance. The ST segment findings
may be transient or elicited only with pharmacologic stimulation or
exertion.
Any patient with unexplained syncope and a Brugada pattern ECG
requires admission for consideration of an implanted defibrillator.
For patients in whom a Brugada pattern ECG is noted incidentally,
there is no consensus on treatment, but we recommend referral to a
cardiologist.
DISPOSITION
Patients with dysrhythmias that are symptomatic and nonresponsive
to ED therapy require admission. Outpatient ambulatory monitoring
and close contact with a cardiologist is an option for patients with no
evidence of structural heart disease who are asymptomatic or only
have palpitations and for patients whose dysrhythmias resolve.4,6
When evaluating anyone with symptomatic rhythm changes, we
recommend a cardiology consultation. Those with VT, torsades de
pointes, type II second-­degree block, or complete heart block require
admission.
The references for this chapter can be found online at ExpertConsult.
com.
918 PART III  Emergency Medicine by System

P P P

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

A II

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II
B

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II
C
Fig. 65.36  Ventricular tachycardia. (A) RS complexes are present in chest leads, but RS duration is greater
than 100 ms. Although the Brugada criteria indicate that no further analysis is necessary, atrioventricular dis-
sociation is also evident, and QRS morphology in lead V6 is consistent with ventricular tachycardia. (B) Some
RS complexes are present, RS duration is no longer than 100 msec, and atrioventricular dissociation is difficult
to appreciate. The morphologic criteria for ventricular tachycardia are fulfilled because S is notched in V1 and
QR is present in V6. (C) Diagnosis is based on morphologic criteria because S is notched in V1 and V2 and QS
are present in V6. (Courtesy Dr. Edward Curtis.)
 CHAPTER 65  Dysrhythmias 919

V2

V6

Fig. 65.37  Bidirectional ventricular tachycardia in a patient with digoxin toxicity. (From Marriott HJL, Conover
MB. Advanced concepts in dysrhythmias. ed 2. St. Louis: Mosby; 1989.)

Fig. 65.38  Torsades de pointes with the classic spiraling of QRS complexes around the baseline.

BOX 65.13  Classification and Causes of Prolonged QT Syndromes That Produce Torsades de Pointes
Pause-­Dependent (Acquired)
Drug-­induced—class IA and IC antidysrhythmics; many phenothiazines and
butyrophenones (notably haloperidol and droperidol), cyclic antidepressants,
antibiotics (especially macrolides), organophosphates, antihistamines, anti-
fungals, antiseizure and antiemetic agents
Electrolyte abnormalities—hypokalemia, hypomagnesemia, hypocalcemia
(rarely)
Diet-­related—starvation, low protein
Severe bradycardia or atrioventricular block
Hypothyroidism
Contrast injection
Cerebrovascular accident (especially intraparenchymal)
Myocardial ischemia
Adrenergic-­Dependent (Tachycardia-­Prompted)
Congenital
Jervell and Lange-­Nielsen syndrome (deafness, autosomal recessive)
Romano–Ward syndrome (normal hearing, autosomal dominant)
Sporadic (normal hearing, no familial tendency)
Mitral valve prolapse
Acquired (Rare)
Cerebrovascular disease (especially subarachnoid hemorrhage)
Autonomic surgery: radical neck dissection, carotid endarterectomy, truncal
vagotomy
920 PART III  Emergency Medicine by System

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V1
A

10 mm/mV 25 mm/s Average

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

B
Fig. 65.39  Brugada syndrome, with ST elevation in V1S. The ST elevation is coved (upper, (A) or saddleback
(lower, (B) and may be transient.