Multiprofessional Critical Care Review Course - 2005
DISTURBANCES OF CARDIAC RHYTHM: TACHYARRHYTHMIAS
OBJECTIVES
• Understand the basic mechanisms of arrhythmias
• Understand the basic types of supraventricular arrhythmias
and their treatments
• Understand the basic assessment of wide complex tachy- ECG criteria: Atrial tachycardia is characterized by an
cardias
• Understand the basic management of atrial fibrillation morphology is distinctly different from that of sinus rhythm,
• Understand the basic treatment of ventricular tachycardia and the PR interval is usually greater than 0.12 milliseconds
and fibrillation
Key Words: atrial fibrillation, atrial flutter, atrioventricu-
lar nodal reentrant tachycardia, orthodromic reciprocating
tachycardia, ventricular fibrillation, ventricular tachycardia,
Wolff-Parkinson-White syndrome
MECHANISMS OF TACHARRHYTHMIAS
The mechanisms of tachyarrhythmias are as follows:
• Abnormal automaticity: This mechanism involves impulse
generation from cells that are not normally arrythmo-
genic.
• Triggered automaticity: This mechanism is attributable
to secondary depolarizations that arise during or after
repolarization.
• Reentry: Reentry is the most commonly encountered
mechanism. The genesis and propagation of an arrhyth-
mia requires the presence of an area of slowed or delayed
conduction, an anatomical or functional separate path
of conduction and unidirectional block. Sites of reentry
include the atria, perinodal tissues, and ventricles.
REGULAR SUPRAVENTRICULAR
TACHYARRHYTHMIAS
Sinus Tachycardia
Electrocardiogram (ECG) criteria: With sinus tachycardia,
the P wave morphology is upright in leads I, II, and aVF.
There is a P wave before every QRS complex and constant
P-R intervals. The rate is not fixed; it varies with sympa-
thetic/parasympathetic stimulus.
Clinical setting: The clinical setting includes catecholamines
(cocaine, amphetamines), fever, hypotension, hypoperfusion,
anxiety/fear, and tricyclic antidepressants (TCA, phenothi-
azines, antihistamines).
Treatment: The preferred treatment is to treat the underly-
ing disorder.
Sarah A. Stahmer, MD, FACEP
Atrial Tachycardia
The second type of regular supraventricular tachycardia is
atrial tachycardia, which is shown in Figure 1.
atrial rate of 150 to 250 beats per minute (bpm). The P wave
(msec). Atrioventricular node (AVN) is not necessary for
rhythm maintenance. Administration of adenosine may cause
AVN blockade, and the atrial tachycardia may be sustained
or may abruptly terminate.
Clinical Setting: The mechanism of atrial tachycardia is
frequently related to associated comorbidities.
• Incisional reentrant atrial tachycardia is seen in patients
with a history of cardiac surgery. It is characterized by
abrupt onset and termination.
• Focal atrial tachycardia is initiated and sustained by a
nonsinus atrial focus. Episodes are usually prolonged, and
the rhythm will typically “warm up” at onset. It is usually
associated with digoxin toxicity, particularly when also
associated with atrioventricular block (AVB). It is also
seen in cardiomyopathy.
Treatment: Treatment depends on the underlying etiology
and frequently requires antiarrhythmic therapy or ablation.
Rate control may be difficult, and response to β-blockers or
calcium channel blockers is unpredictable.
Atrial Flutter
The third type of regular supraventricular tachyarrhythmia
is atrial flutter (Figure 2).
Recognition: Atrial flutter generally has an atrial rate be-
tween 250 and 350 bpm and ventricular rates one half to one
third the flutter rate. Occasionally, atrial flutter presents with
a variable ventricular response. Atrial flutter is a circuit that
typically rotates in a counterclockwise fashion around the
right atrium and has a negative saw-tooth pattern in inferior
leads II and aVF and positive flutter waves in lead VI. It
is usually regular in untreated patients. Clinical pearl: An
unchanging ventricular rate of 148-150 is atrial flutter with
2:1 block until proven otherwise.
Clinical setting: This includes acute myocardial infarction
(MI)/ischemic heart disease, congestive cardiomyopathy,
pulmonary embolism (PE), and myocarditis.
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Figure 1. Atrial tachycardia

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Figure 2. Atrial Flutter

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Figure 3. Paroxysmal supraventricular tachycardia: AV nodal reentrant tachycardia
Treatment: With atrial flutter, the rhythm is inherently
unstable and will convert to normal sinus rhythm (NSR)
or atrial fibrillation (Afib). For unstable patients, synchro-
nized cardioversion is 25-50 J. For stable patients, control
the ventricular rate with diltiazem, β-blockers, or digoxin.
Never use Type Ia antiarrhythmics before ventricular rate
is controlled. (They will enhance AV conduction and may
result in 1:1 conduction.)
Paroxysmal Supraventricular Tachycardia:
AV Nodal Reentrant Tachycardia
The final type of regular supraventricular tachyarrhythmia
(SVT) is paroxysmal supraventricular tachycardia. AV nodal
reentrant tachycardia (AVNRT, Figure 3) is one of the sub-
categories of this type of tachycardia.
Recognition: This type of tachycardia is characterized by
regular, rapid rhythm with ventricular rates ranging from
140-280 beats/minute (bpm). The QRS is narrow, unless
there is a preexisting bundle branch block (BBB) or rate-
related bundle. Most reentrant arrhythmias are triggered by
4
a premature atrial contraction (PAC) that blocks down the
fast pathway (which has a long refractory period) and con-
ducts down the slow pathway ( which has a short refractory
period). The atrium is depolarized retrograde, and the P wave
is usually buried. When the P-wave is seen, it suggests that
the reentry pathway is conducting retrograde via the slow
pathway, or via a bypass tract.
Clinical setting: The precipitating event in reentrant tachy-
cardias is usually a premature atrial beat, so any process
that causes PACs will put the patient at risk. These include
processes that result in atrial stretch (acute coronary syn-
drome [ACS], congestive heart failure [CHF]), irritability
(exogenous catecholamines), and irritation (pericarditis).
Treatment: Typical treatment includes vagal maneuvers,
adenosine (this is the drug of choice), diltiazem, or β-block-
ers. Unstable patients should be synchronously cardioverted
at 25-50 J.
 Multiprofessional Critical Care Review Course - 2005
Figure 4. Orthodromic reciprocating tachycardia
Paroxysmal Supraventricular Tachycardia:
Orthodromic Reciprocating Tachycardia
The other subcategory of paroxysmal supraventricular tachy-
cardia is known as orthodromic reciprocating tachycardia
(ORT) (Figure 4).
Recognition: ORT is a narrow complex tachycardia. An-
terograde (forward) conduction occurs via the normal AV
nodal conduction system with retrograde conduction via a
concealed accessory pathway. The PR interval is forcibly
longer than with AVNRT because of slow retrograde conduc-
tion up the accessory pathway.
Clinical setting: The clinical setting is similar to that of
AVNRT.
Treatment: The treatment is similar to that for AVNRT. Be-
cause this dysrhythmia it is obligated to use the AV node for
anterograde conduction, it is amenable to AV nodal blocking
agents for acute and chronic therapy. However, pharmaco-
logic therapy is frequently less than adequately effective, and
recurrences on medical therapy are common. This arrhythmia
is also very amenable to catheter ablation, which has a 95%
success rate and a low complication rate.
IRREGULAR SUPRAVENTRICULAR
TACHYARRHYTHMIAS
Multifocal Atrial Tachycardia
The first type of irregular supraventricular tachyarrhythmia
discussed in this chapter is the multifocal atrial tachycardia
(Figure 5).
Recognition: Multifocal atrial tachycardia is a narrow com-
plex, irregular tachycardia that is attributable to abnormal
automaticity of multiple atrial foci. The P waves will dem-
onstrate at least three different morphologies, with variable
PR intervals. The atrial rate varies from 100-180 bpm.
Clinical Setting: Multifocal atrial tachycardia is typically
seen in patients with acute exacerbations of chronic obstruc-
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Figure 5. Multifocal atrial tachycardia
tive pulmonary disease. It is occasionally associated with
CHF, sepsis, and theophylline toxicity.
Treatment: Treat the underlying disorder! Antidysrhythmics
are usually not helpful in treating multifocal atrial tachy-
cardia. Intravenous (IV) magnesium (which may reduce
atrial ectopy) and IV verapamil/diltiazem may decrease the
ventricular response rate, and amiodarone may restore sinus
rhythm. The rhythm will usually abate once the underlying
(usually respiratory) disorder is treated.
Atrial Fibrillation
Atrial fibrillation is one of the most common atrial arrhyth-
mias (Figure 6).
Recognition: Atrial fibrillation is characterized by a lack of
organized atrial activity. On the ECG it manifests as a lack
of clear P waves between QRS complexes and an irregular
ventricular response. Atrial fibrillation has now been shown
to be attributable to multiple reentrant wavelets conducting
between the right and left atrium.
6
• Baseline wavers without P waves (the atria never uniformly
depolarize)
• Ventricular rate determined by degree of AV conduction
(untreated usually > 170 bpm)
• QRS usually narrow unless there is a preexisting BBB or,
after a long R-R interval, a beat is conducted with a short
R-R interval and is aberrant (Ashman’s phenomenon).
Clinical Setting: Ischemic heart disease (with or without
infarction), hypertension, thyrotoxicosis, “holiday heart,”
pericarditis
Treatment: Acute management of atrial fibrillation initially
focuses on rate control and anticoagulation. Rate control is
usually achieved through the use of calcium channel blockers,
β-blockers, amiodarone, and digoxin to slow the ventricular
response. Digoxin and amiodarone may be particularly effec-
tive in light of their lack of negative inotropic effect.
Emergent cardioversion: Emergent cardioversion is indicat-
ed in the setting of severe refractory congestive heart failure,
intractable angina, or refractory hypotension when ventricular
 Multiprofessional Critical Care Review Course - 2005
Figure 6. Atrial fibrillation
response cannot be controlled. Unstable patients may be
cardioverted (synchronized) beginning at 100-200 J.
Elective cardioversion: Patients with duration of atrial
fibrillation less than 48 hours may generally undergo
cardioversion to normal sinus rhythm with minimal risk of
thromboembolism. The rate of embolism with cardioversion
within 48 hours without prior anticoagulation is estimated
to be approximately 0.8%. Pharmacologic therapy for acute
conversion to sinus rhythm may also be performed within
48 hours.
Chemical conversion (after slowing VR): Procainamide,
disopyramide, propafenone, sotalol, flecainide, amiodarone,
and ibutilide. A newer agent is dofetilide, a recently approved
class III antiarrhythmic.
Anticoagulation: Atrial fibrillation is known to be associated
with increased risk of stroke and death. The risk of thrombo-
embolism in nonanticoagulated patients is between 5% and
6% per year but may be as high as 20% in certain populations,
including the elderly and those with certain valvular lesions
(i.e., mitral stenosis).
WIDE COMPLEX TACHYCARDIAS
Polymorphic VT
Defined as a QRS complex greater than 120 msec with rate
greater than 100 beats per minute. The differential diagnosis
includes SVT with aberrancy, accessory pathway conduc-
tion, pre-excitation syndrome (e.g., Wolff-Parkinson-White
syndrome [WPW]) or ventricular tachycardia (VT). The
majority of patients presenting with a wide complex tachy-
cardia will be diagnosed with VT; if the patient has a history
of coronary artery disease the incidence increases to 95%.
Careful inspection of the 12-lead ECG will allow correct
determination of the diagnosis in approximately 90% of
patients. Despite this fact, VT is frequently misinterpreted as
being supraventricular tachycardia with aberrancy. Common
errors include the assumption that VT cannot be “narrow,”and
that it cannot occur in an awake patient. In addition, there
is a lack of familiarity with ECG criteria for VT. See Table
1 for an algorithm demonstrating steps in diagnosing wide
QRS-complex tachycardia.
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 Multiprofessional Critical Care Review Course - 2005
Table 1. Diagnosis of wide QRS complex tachycardia with
a regular rhythm
ECG criteria: A number of decision rules have been pro-
posed in an attempt to identify features on the 12-lead ECG
that will aid in the diagnosis of VT. The criteria vary in their
reliability when applied individually and must be interpreted
in conjunction with the other criteria—and with the patient’s
clinical presentation, medical history, and previous ECG
when available. A frequently used diagnostic algorithm
by Brugada et al incorporates many previously published
morphology criteria in a stepwise algorithm (see Table 2);
it has been demonstrated to be very sensitive and specific
in the absence of preexisting intraventricular conduction
abnormalities. Wide complex tachycardias are divided into
right and left bundle branch type. If the complex is upright
in lead V1 of a standard 12-lead ECG then it is defined as a
right bundle branch type. If the complex is negative in lead
V1 then it is defined as a left bundle branch type.
Clinical setting: Sustained VT is defined as VT lasting
greater than 30 seconds. The rhythm can originate from any
part of the myocardium and/or conduction system below the
atrioventricular node. VT is frequently seen as a complication
of coronary artery disease (CAD) due to active ischemia or
presence of scar tissue, both of which can create substrates
for ventricular arrhythmias. Patients with cardiomyopathies,
particularly the idiopathic dilated type, are the second largest
group of patients at risk for developing VT. However, VT
can also occur (although rarely) in healthy people, or it may
be the first indication of organic heart disease, for example,
right ventricular dysplasia. Medications, particularly some
antiarrhythmic therapies can be proarrhythmic under certain
clinical conditions, and give rise to ventricular arrhythmias.
8
They include digoxin, Type I antiarrhythmics, phenothi-
azines, tricyclic antiarrhythmics, and sympathomimetics.
Medications that cause prolongation of the QT interval
can generate a specific polymorphic form of VT known
as torsades de pointes. Finally, severe or acute electrolyte
imbalances, particularly hypokalemia and hyperkalemia,
can give rise to VT.
Treatment: The new Advanced Cardiac Life Support (ACLS)
guidelines differentiate the treatment of VT in patients with
normal left ventricular function from those with diminished
function. For patients with depressed left ventricular func-
tion, the pharmacologic treatment of choice is IV amiodarone
administered as a 150-mg bolus over 10 minutes. It has been
successfully used for out-of-hospital cardiac arrests with a
300-mg IV bolus. In patients with preserved left ventricular
function and wide complex arrhythmia of unknown etiology or
VT, acceptable choices of therapy include DC cardioversion,
amiodarone, or procainamide. For every tachyarrhythmia,
amiodarone may be used as a primary or secondary choice.
Lidocaine is now considered secondary in therapy as a result of
its limited effectiveness in ventricular tachycardia in nonisch-
emic tissue. It should be noted that the use of combination
antiarrhythmic therapy is strongly discouraged because of a
proarrhythmic potential and limited efficacy.
DC cardioversion is a universally acceptable treatment
option, and it should be considered whenever a patient is
hemodynamically unstable, fails to respond to antiarrhythmic
therapy, or is experiencing chest pain or its equivalent. Proper
sedation should always be provided before cardioversion.
Polymorphic VT: Torsades de Pointes:
Prolonged QT Interval
Recognition: Torsades de pointes (see Figure 7) is a rapid
polymorphic VT that is characterized by beat-to-beat vari-
ability in the QRS complexes, which vary in both amplitude
and polarity. The resultant QRS complexes appear to “twist”
around the isoelectric line. A prerequisite for the rhythm
is baseline prolongation of the QT interval, which may be
congenital or acquired. Torsades is initiated by a series of
ectopic beats that begin with a premature ventricular beat
or salvo of ventricular beats, followed by a pause, and then
a supraventricular beat. Another premature ventricular beat
arrives at a relatively short coupling interval and falls on the
preceding T wave, precipitating the rhythm.
Torsades is usually paroxysmal in nature, and the underlying
rhythm and intervals can be identified during “breaks” in the
rhythm. Typically, there are 5 to 20 complexes in each cycle,
and the rhythm self-terminates or degenerates into ventricular
fibrillation. The ventricular rate is usually between 200 and
250 bpm, and the amplitude of the QRS complexes will vary
in a sinusoidal pattern.The baseline ECG will usually provide
important clues to the nature of the arrhythmia. Because the
QT interval lengthens with decreasing heart rate, measure-
 Multiprofessional Critical Care Review Course - 2005

ment of a rate-independent QT interval may be calculated. Table 2. Morphology criteria for ventricular tachycar-
The standard correction for rate is the QT interval divided by dia*
the square root of the R-R interval measured in milliseconds.
The presence of a corrected QT interval of greater than 440-
450 milliseconds should be considered abnormal. Patients
with QT intervals corrected for rate greater than 500 mil-
liseconds, and certainly 600 milliseconds, have been shown
to be at increased risk for torsades de pointes. In addition to
prolongations of the corrected QT interval (QTc), there may
be changes in the ST segment and T wave that would provide
clues to an underlying metabolic abnormality.

Clinical Setting: Acquired causes of QT prolongation are

by far the most common, with medications (type Ia anti-
arrhythmics) and electrolyte imbalances (hypokalemia,
hypomagnesemia) the most frequent culprits.

Some patients present with syncope or sudden death and

are found to have polymorphic VT, torsades de pointes,
and a prolonged QT interval without any clear predisposing
medication or condition. These patients have congenital long
QT syndrome.

Treatment: Treatment of torsades in the setting of acquired

long QT syndrome leading to torsades de pointes consists
of removing offending agents or conditions. Further therapy
includes treatment with IV magnesium, which prevents the
onset of torsades de pointes. Temporary pacing or admin-
istering isoproterenol increases the underlying heart rate
and shortens the QT interval. Therapy for symptomatic
congenital long QT syndrome is considered to consist of
β-blocker therapy and pacing. Some advocate a left stellate
ganglionectomy.
Right ventricular outflow tract ventricular tachycardia
(RVOT-VT): This form of VT (see Figure 8) is seen in
patients without underlying heart disease. It originates from
or near the right ventricular outflow tract and, typically, has
a left bundle branch block (LBBB) morphology and right
inferior axis.
Patients will present with palpitations or syncope, and trig-
gers are thought to be exercise and other causes of increased
adrenergic tone. It typically responds to β-blockers or cal-
cium-channel blockade. It has been reported to respond to
adenosine, and it can be misinterpreted as supraventricular
tachycardia with aberrancy.
Ventricular Fibrillation
Recognition: For ventricular fibrillation (VF) the ECG shows
complexes that are grossly irregular without P waves or clear
QRS morphology (see Figure 9).
Clinical Setting: This rhythm does not generate meaningful
cardiac contractions, and the patient is always unconscious.
VF is seen in patients with severe ischemic heart disease,
acute MI, hypothermia, blunt chest trauma.
Treatment: VF is treated by immediate defibrillation. This
process should be repeated if the first attempt is unsuccess-
ful. Amiodarone 300 mg IVP if the patient fails to respond
to defibrillation 3 times and fails to cardiovert. Rewarming
should be initiated if the patient becomes hypothermic.
PRE-EXCITATION SYNDROMES

Polymorphic VT: Normal QT Interval WPW Syndrome

This form of VT will often appear as torsade, the difference
is the absence of QT prolongation. Patients with this rhythm
are often found to have unstable coronary artery disease,
and acute myocardial ischemia is felt to be an important
prerequisite for this arrhythmia. These patients are usually
unstable, and DC cardioversion is the treatment of choice.
Recognition: With WPW syndrome, the baseline ECG when
the patient is in sinus rhythm is a short PR interval and “delta”
wave—a slurring of the upstroke of the R wave. There are
associated ST-T changes secondary to altered depolariza-
tion/repolarization. A predisposition to tachydysrhythmias
is associated with WPW syndrome; atrial flutter (5%), atrial

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Figure 7. Polymorphic ventricular tachycardia: Torsades de pointes

Figure 8. Right ventricular outflow tract ventricular tachycardia

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Figure 9. Ventricular fibrillation

Figure 10. Wolff-Parkinson-White syndrome, a pre-excitation syndrome

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Figure 11. Atrial fibrillation and flutter in the setting of Wolff-Parkinson-White syndrome
fibrillation (10% to 20%), and paroxysmal SVT (40% to 80%)
are the most common (see Figure 10).
Clinical Setting: WPW is the most common form of pre-ex-
citation. The cause of this abnormal ventricular depolarization
is the presence of one or more accessory pathways. These ac-
cessory pathways are small bands of tissue, called the Kent’s
bundle, that failed to separate during development, thereby al-
lowing continued electrical conduction between the atria and
ventricles at sites other than at the AV node. The accessory
pathway conduction circumvents the usual conduction delay
between the atria and ventricles that occurs within the AV
node. This leads to early eccentric activation of the ventricles
with subsequent fusion with the usual AV nodal conduction.
These pathways may allow rapid conduction from the atria
to the ventricle, which may predispose patients to a risk of
sudden death from ventricular fibrillation.
Treatment: Treatment of the dysrhythmia requires one to
identify the underlying rhythm, and then understand the
implications of “usual treatment” in the presence of a bypass
tract. The key difference lies in rhythms that do not depend
on the AVN for perpetuation, such as atrial fibrillation and
flutter. Usual treatment in these rhythms consists of control-
ling the ventricular rate with agents that block the AVN. In
12
the setting of a bypass tract, blocking the AVN will result in
impulse conduction down the accessory pathway, which does
not have the inherent refractoriness that the AVN has. The
pathway can conduct atrial rates in excess of 300 bpm, which
can precipitate degeneration into ventriculoar fibrillation.
Atrial fibrillation and flutter in the setting
of WPW
Atrial fibrillation and flutter are less commonly seen in as-
sociation with WPW, and yet are the most feared (Figure
11). In both atrial fibrillation and flutter, atrial depolarization
rates are equal to or greater than 300 bpm. Atrial impulses
are blocked at the AV node because of its relatively long
refractory period, and concealed conduction and ventricular
response rates are much slower. Accessory pathways have
significantly shorter refractory periods and faster conduction
time compared to the AV node, and in these rhythms, nearly
all atrial depolarizations are conducted down the accessory
pathway. The pattern of ventricular activation will vary
dependent on the relative proportion of electrical activation
conducted via the AV node and accessory pathway, resulting
in widened and bizarre-appearing QRS complexes that vary
in width on a beat-to-beat basis.
 Multiprofessional Critical Care Review Course - 2005
Figure 12. Orthodromic, reentrant supraventricular tachycardia
The appearance of atrial fibrillation in the setting of a bypass
tract can easily be confused with polymorphic VT or atrial
fibrillation with rate-related aberrancy. The ventricular re-
sponse in polymorphic VT is never as grossly irregular as
atrial fibrillation. Inspection of the ECG in atrial fibrillation
in WPW will also show that the QRS is usually relatively
narrow at the shortest R-R intervals (fastest heart rates) due
to sole conduction down the bypass tract. This is because
the AV node cannot conduct at ventricular response rate
approaching 300 bpm, whereas the bypass tract can. This
is also in direct contrast to rate-related aberrancy, where
the QRS complexshould be most aberrant at the shortest
R-R intervals.
Usual treatment of atrial fibrillation (without an accessory
pathway) consists of cardioversion for unstable patients.
For stable patients the ventricular response is controlled
with agents that block the AVN. Cardioversion of the atrial
fibrillation is still the intervention of choice for unstable
patients, and the presence of an accessory pathway does not
alter this. For the stable patient with an accessory pathway,
blocking the AVN will result in impulse conduction entirely
down the accessory pathway. The pathway has the potential to
conduct at rates in excess of 300 bpm, which can precipitate
degeneration into ventricular fibrillation. The treatment is to
slow conduction through the bypass tract, which is usually
accomplished with procainamide and amiodarone.
Orthodromic, Reentrant SVT
Orthodromic, reentrant SVT will appear as a narrow com-
plex, regular tachycardia. Drugs or maneuvers that slow
AV conduction can be used, where even in the presence
of a bypass tract the AVN is an integral component of the
reentrant pathway. Blocking the AVN will abruptly “break”
the rhythm.
Antidromic wide complex SVT
Because of antegrade conduction down the bypass tract, the
rhythm will be regular and will have wide QRS complexes.
Agents that block the AVN will be effective in breaking the
reentrant circuit, but the clinician must be sure of the rhythm
interpretation. When in doubt, a trial of adenosine is often
helpful. If the rhythm fails to “break,” then procainamide or
amiodarone are reasonable choices.
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Figure 13. Pacemaker-mediated tachycardia
Pacemaker-Mediated Tachycardia
Recognition: Regular, rapid, wide complex rhythm in a
patient with a DDD (dual pacing, sensing, and inhibition)
pacemaker.
Clinical setting: This is a reentrant tachycardia that occurs
when sensing of a retrograde atrial depolarization triggers
ventricular pacing and is sustained by the pacemaker. It is
usually initiated by a premature ventricular contraction,
which is conducted retrograde to the atria and is subsequently
sensed by the pacemaker.
Treatment: Application of a magnet converts the pacer to
the DOO (pacing function only) mode, which disrupts the
sensing function of the pacemaker and terminates the rhythm.
The rhythm will not recur once the magnet is removed. If the
rhythm does reoccur, then the rhythm is likely to be atrial flut-
ter where the ventricular response rate is at the programmed
upper limit of the pacemaker.
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 Multiprofessional Critical Care Review Course - 2005
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Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia:
misdiagnosis and outcome after emergent therapy. Ann Intern
Med. 1986;104:766-771.
Description of common misdiagnoses of wide complex tachy-
cardias and cliical outcomes.
Trohman RG. Supraventricular tachycardia: implications for the
intensivist. Crit Care Med. 2000;28(10 Suppl):N129-N135
An excellent review of SVT, including recognition, mecha-
nisms, precipitants, and treatment of commonly encountered
rhythms.
Wellens HJ, Brugada P. Diagnosis of ventricular tachycardia from
the 12-lead Eeectrocardiogram. Cardiol Clin. 1987;5: 511-
525.
Classic article describing findings on the 12-lead ECG that
will identify patients with VT as the cause of their wide
complex tachycardia.
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