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Multiprofessional Critical Care Review Course - 2005


Sarah A. Stahmer, MD, FACEP

OBJECTIVES Atrial Tachycardia

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

Multiprofessional Critical Care Review Course - 2005

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 a premature atrial contraction (PAC) that blocks down the
unstable and will convert to normal sinus rhythm (NSR) fast pathway (which has a long refractory period) and con-
or atrial fibrillation (Afib). For unstable patients, synchro- ducts down the slow pathway ( which has a short refractory
nized cardioversion is 25-50 J. For stable patients, control period). The atrium is depolarized retrograde, and the P wave
the ventricular rate with diltiazem, β-blockers, or digoxin. is usually buried. When the P-wave is seen, it suggests that
Never use Type Ia antiarrhythmics before ventricular rate the reentry pathway is conducting retrograde via the slow
is controlled. (They will enhance AV conduction and may pathway, or via a bypass tract.
result in 1:1 conduction.)
Clinical setting: The precipitating event in reentrant tachy-
Paroxysmal Supraventricular Tachycardia: cardias is usually a premature atrial beat, so any process
AV Nodal Reentrant Tachycardia that causes PACs will put the patient at risk. These include
processes that result in atrial stretch (acute coronary syn-
The final type of regular supraventricular tachyarrhythmia drome [ACS], congestive heart failure [CHF]), irritability
(SVT) is paroxysmal supraventricular tachycardia. AV nodal (exogenous catecholamines), and irritation (pericarditis).
reentrant tachycardia (AVNRT, Figure 3) is one of the sub-
categories of this type of tachycardia. Treatment: Typical treatment includes vagal maneuvers,
adenosine (this is the drug of choice), diltiazem, or β-block-
Recognition: This type of tachycardia is characterized by ers. Unstable patients should be synchronously cardioverted
regular, rapid rhythm with ventricular rates ranging from at 25-50 J.
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

Multiprofessional Critical Care Review Course - 2005

Figure 4. Orthodromic reciprocating tachycardia

Paroxysmal Supraventricular Tachycardia: recurrences on medical therapy are common. This arrhythmia
Orthodromic Reciprocating Tachycardia is also very amenable to catheter ablation, which has a 95%
success rate and a low complication rate.
The other subcategory of paroxysmal supraventricular tachy-
cardia is known as orthodromic reciprocating tachycardia IRREGULAR SUPRAVENTRICULAR

Recognition: ORT is a narrow complex tachycardia. An- Multifocal Atrial Tachycardia

terograde (forward) conduction occurs via the normal AV
nodal conduction system with retrograde conduction via a The first type of irregular supraventricular tachyarrhythmia
concealed accessory pathway. The PR interval is forcibly discussed in this chapter is the multifocal atrial tachycardia
longer than with AVNRT because of slow retrograde conduc- (Figure 5).
tion up the accessory pathway.
Recognition: Multifocal atrial tachycardia is a narrow com-
Clinical setting: The clinical setting is similar to that of plex, irregular tachycardia that is attributable to abnormal
AVNRT. automaticity of multiple atrial foci. The P waves will dem-
onstrate at least three different morphologies, with variable
Treatment: The treatment is similar to that for AVNRT. Be- PR intervals. The atrial rate varies from 100-180 bpm.
cause this dysrhythmia it is obligated to use the AV node for
anterograde conduction, it is amenable to AV nodal blocking Clinical Setting: Multifocal atrial tachycardia is typically
agents for acute and chronic therapy. However, pharmaco- seen in patients with acute exacerbations of chronic obstruc-
logic therapy is frequently less than adequately effective, and

Multiprofessional Critical Care Review Course - 2005

Figure 5. Multifocal atrial tachycardia

tive pulmonary disease. It is occasionally associated with • Baseline wavers without P waves (the atria never uniformly
CHF, sepsis, and theophylline toxicity. depolarize)
• Ventricular rate determined by degree of AV conduction
Treatment: Treat the underlying disorder! Antidysrhythmics (untreated usually > 170 bpm)
are usually not helpful in treating multifocal atrial tachy- • QRS usually narrow unless there is a preexisting BBB or,
cardia. Intravenous (IV) magnesium (which may reduce after a long R-R interval, a beat is conducted with a short
atrial ectopy) and IV verapamil/diltiazem may decrease the R-R interval and is aberrant (Ashman’s phenomenon).
ventricular response rate, and amiodarone may restore sinus
rhythm. The rhythm will usually abate once the underlying Clinical Setting: Ischemic heart disease (with or without
(usually respiratory) disorder is treated. infarction), hypertension, thyrotoxicosis, “holiday heart,”
Atrial Fibrillation
Treatment: Acute management of atrial fibrillation initially
Atrial fibrillation is one of the most common atrial arrhyth- focuses on rate control and anticoagulation. Rate control is
mias (Figure 6). usually achieved through the use of calcium channel blockers,
β-blockers, amiodarone, and digoxin to slow the ventricular
Recognition: Atrial fibrillation is characterized by a lack of response. Digoxin and amiodarone may be particularly effec-
organized atrial activity. On the ECG it manifests as a lack tive in light of their lack of negative inotropic effect.
of clear P waves between QRS complexes and an irregular
ventricular response. Atrial fibrillation has now been shown Emergent cardioversion: Emergent cardioversion is indicat-
to be attributable to multiple reentrant wavelets conducting ed in the setting of severe refractory congestive heart failure,
between the right and left atrium. 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 WIDE COMPLEX TACHYCARDIAS

cardioverted (synchronized) beginning at 100-200 J.
Polymorphic VT
Elective cardioversion: Patients with duration of atrial
fibrillation less than 48 hours may generally undergo Defined as a QRS complex greater than 120 msec with rate
cardioversion to normal sinus rhythm with minimal risk of greater than 100 beats per minute. The differential diagnosis
thromboembolism. The rate of embolism with cardioversion includes SVT with aberrancy, accessory pathway conduc-
within 48 hours without prior anticoagulation is estimated tion, pre-excitation syndrome (e.g., Wolff-Parkinson-White
to be approximately 0.8%. Pharmacologic therapy for acute syndrome [WPW]) or ventricular tachycardia (VT). The
conversion to sinus rhythm may also be performed within majority of patients presenting with a wide complex tachy-
48 hours. cardia will be diagnosed with VT; if the patient has a history
of coronary artery disease the incidence increases to 95%.
Chemical conversion (after slowing VR): Procainamide, Careful inspection of the 12-lead ECG will allow correct
disopyramide, propafenone, sotalol, flecainide, amiodarone, determination of the diagnosis in approximately 90% of
and ibutilide. A newer agent is dofetilide, a recently approved patients. Despite this fact, VT is frequently misinterpreted as
class III antiarrhythmic. being supraventricular tachycardia with aberrancy. Common
errors include the assumption that VT cannot be “narrow,”and
Anticoagulation: Atrial fibrillation is known to be associated that it cannot occur in an awake patient. In addition, there
with increased risk of stroke and death. The risk of thrombo- is a lack of familiarity with ECG criteria for VT. See Table
embolism in nonanticoagulated patients is between 5% and 1 for an algorithm demonstrating steps in diagnosing wide
6% per year but may be as high as 20% in certain populations, QRS-complex tachycardia.
including the elderly and those with certain valvular lesions
(i.e., mitral stenosis).

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Table 1. Diagnosis of wide QRS complex tachycardia with They include digoxin, Type I antiarrhythmics, phenothi-
a regular rhythm 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.

ECG criteria: A number of decision rules have been pro- DC cardioversion is a universally acceptable treatment
posed in an attempt to identify features on the 12-lead ECG option, and it should be considered whenever a patient is
that will aid in the diagnosis of VT. The criteria vary in their hemodynamically unstable, fails to respond to antiarrhythmic
reliability when applied individually and must be interpreted therapy, or is experiencing chest pain or its equivalent. Proper
in conjunction with the other criteria—and with the patient’s sedation should always be provided before cardioversion.
clinical presentation, medical history, and previous ECG
when available. A frequently used diagnostic algorithm Polymorphic VT: Torsades de Pointes:
by Brugada et al incorporates many previously published Prolonged QT Interval
morphology criteria in a stepwise algorithm (see Table 2);
it has been demonstrated to be very sensitive and specific Recognition: Torsades de pointes (see Figure 7) is a rapid
in the absence of preexisting intraventricular conduction polymorphic VT that is characterized by beat-to-beat vari-
abnormalities. Wide complex tachycardias are divided into ability in the QRS complexes, which vary in both amplitude
right and left bundle branch type. If the complex is upright and polarity. The resultant QRS complexes appear to “twist”
in lead V1 of a standard 12-lead ECG then it is defined as a around the isoelectric line. A prerequisite for the rhythm
right bundle branch type. If the complex is negative in lead is baseline prolongation of the QT interval, which may be
V1 then it is defined as a left bundle branch type. congenital or acquired. Torsades is initiated by a series of
ectopic beats that begin with a premature ventricular beat
Clinical setting: Sustained VT is defined as VT lasting or salvo of ventricular beats, followed by a pause, and then
greater than 30 seconds. The rhythm can originate from any a supraventricular beat. Another premature ventricular beat
part of the myocardium and/or conduction system below the arrives at a relatively short coupling interval and falls on the
atrioventricular node. VT is frequently seen as a complication preceding T wave, precipitating the rhythm.
of coronary artery disease (CAD) due to active ischemia or
presence of scar tissue, both of which can create substrates Torsades is usually paroxysmal in nature, and the underlying
for ventricular arrhythmias. Patients with cardiomyopathies, rhythm and intervals can be identified during “breaks” in the
particularly the idiopathic dilated type, are the second largest rhythm. Typically, there are 5 to 20 complexes in each cycle,
group of patients at risk for developing VT. However, VT and the rhythm self-terminates or degenerates into ventricular
can also occur (although rarely) in healthy people, or it may fibrillation. The ventricular rate is usually between 200 and
be the first indication of organic heart disease, for example, 250 bpm, and the amplitude of the QRS complexes will vary
right ventricular dysplasia. Medications, particularly some in a sinusoidal pattern.The baseline ECG will usually provide
antiarrhythmic therapies can be proarrhythmic under certain important clues to the nature of the arrhythmia. Because the
clinical conditions, and give rise to ventricular arrhythmias. 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 Ventricular Fibrillation
congenital long QT syndrome is considered to consist of
β-blocker therapy and pacing. Some advocate a left stellate Recognition: For ventricular fibrillation (VF) the ECG shows
ganglionectomy. complexes that are grossly irregular without P waves or clear
QRS morphology (see Figure 9).
Right ventricular outflow tract ventricular tachycardia
(RVOT-VT): This form of VT (see Figure 8) is seen in Clinical Setting: This rhythm does not generate meaningful
patients without underlying heart disease. It originates from cardiac contractions, and the patient is always unconscious.
or near the right ventricular outflow tract and, typically, has VF is seen in patients with severe ischemic heart disease,
a left bundle branch block (LBBB) morphology and right acute MI, hypothermia, blunt chest trauma.
inferior axis.
Treatment: VF is treated by immediate defibrillation. This
Patients will present with palpitations or syncope, and trig- process should be repeated if the first attempt is unsuccess-
gers are thought to be exercise and other causes of increased ful. Amiodarone 300 mg IVP if the patient fails to respond
adrenergic tone. It typically responds to β-blockers or cal- to defibrillation 3 times and fails to cardiovert. Rewarming
cium-channel blockade. It has been reported to respond to should be initiated if the patient becomes hypothermic.
adenosine, and it can be misinterpreted as supraventricular
tachycardia with aberrancy. PRE-EXCITATION SYNDROMES

Polymorphic VT: Normal QT Interval WPW Syndrome

This form of VT will often appear as torsade, the difference Recognition: With WPW syndrome, the baseline ECG when
is the absence of QT prolongation. Patients with this rhythm the patient is in sinus rhythm is a short PR interval and “delta”
are often found to have unstable coronary artery disease, wave—a slurring of the upstroke of the R wave. There are
and acute myocardial ischemia is felt to be an important associated ST-T changes secondary to altered depolariza-
prerequisite for this arrhythmia. These patients are usually tion/repolarization. A predisposition to tachydysrhythmias
unstable, and DC cardioversion is the treatment of choice. 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%) the setting of a bypass tract, blocking the AVN will result in
are the most common (see Figure 10). impulse conduction down the accessory pathway, which does
not have the inherent refractoriness that the AVN has. The
Clinical Setting: WPW is the most common form of pre-ex- pathway can conduct atrial rates in excess of 300 bpm, which
citation. The cause of this abnormal ventricular depolarization can precipitate degeneration into ventriculoar fibrillation.
is the presence of one or more accessory pathways. These ac-
cessory pathways are small bands of tissue, called the Kent’s Atrial fibrillation and flutter in the setting
bundle, that failed to separate during development, thereby al- of WPW
lowing continued electrical conduction between the atria and
ventricles at sites other than at the AV node. The accessory Atrial fibrillation and flutter are less commonly seen in as-
pathway conduction circumvents the usual conduction delay sociation with WPW, and yet are the most feared (Figure
between the atria and ventricles that occurs within the AV 11). In both atrial fibrillation and flutter, atrial depolarization
node. This leads to early eccentric activation of the ventricles rates are equal to or greater than 300 bpm. Atrial impulses
with subsequent fusion with the usual AV nodal conduction. are blocked at the AV node because of its relatively long
These pathways may allow rapid conduction from the atria refractory period, and concealed conduction and ventricular
to the ventricle, which may predispose patients to a risk of response rates are much slower. Accessory pathways have
sudden death from ventricular fibrillation. significantly shorter refractory periods and faster conduction
time compared to the AV node, and in these rhythms, nearly
Treatment: Treatment of the dysrhythmia requires one to all atrial depolarizations are conducted down the accessory
identify the underlying rhythm, and then understand the pathway. The pattern of ventricular activation will vary
implications of “usual treatment” in the presence of a bypass dependent on the relative proportion of electrical activation
tract. The key difference lies in rhythms that do not depend conducted via the AV node and accessory pathway, resulting
on the AVN for perpetuation, such as atrial fibrillation and in widened and bizarre-appearing QRS complexes that vary
flutter. Usual treatment in these rhythms consists of control- in width on a beat-to-beat basis.
ling the ventricular rate with agents that block the AVN. In
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Figure 12. Orthodromic, reentrant supraventricular tachycardia

The appearance of atrial fibrillation in the setting of a bypass slow conduction through the bypass tract, which is usually
tract can easily be confused with polymorphic VT or atrial accomplished with procainamide and amiodarone.
fibrillation with rate-related aberrancy. The ventricular re-
sponse in polymorphic VT is never as grossly irregular as Orthodromic, Reentrant SVT
atrial fibrillation. Inspection of the ECG in atrial fibrillation
in WPW will also show that the QRS is usually relatively Orthodromic, reentrant SVT will appear as a narrow com-
narrow at the shortest R-R intervals (fastest heart rates) due plex, regular tachycardia. Drugs or maneuvers that slow
to sole conduction down the bypass tract. This is because AV conduction can be used, where even in the presence
the AV node cannot conduct at ventricular response rate of a bypass tract the AVN is an integral component of the
approaching 300 bpm, whereas the bypass tract can. This reentrant pathway. Blocking the AVN will abruptly “break”
is also in direct contrast to rate-related aberrancy, where the rhythm.
the QRS complexshould be most aberrant at the shortest
R-R intervals. Antidromic wide complex SVT

Usual treatment of atrial fibrillation (without an accessory Because of antegrade conduction down the bypass tract, the
pathway) consists of cardioversion for unstable patients. rhythm will be regular and will have wide QRS complexes.
For stable patients the ventricular response is controlled Agents that block the AVN will be effective in breaking the
with agents that block the AVN. Cardioversion of the atrial reentrant circuit, but the clinician must be sure of the rhythm
fibrillation is still the intervention of choice for unstable interpretation. When in doubt, a trial of adenosine is often
patients, and the presence of an accessory pathway does not helpful. If the rhythm fails to “break,” then procainamide or
alter this. For the stable patient with an accessory pathway, amiodarone are reasonable choices.
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
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Figure 13. Pacemaker-mediated tachycardia

Pacemaker-Mediated Tachycardia BIBLIOGRAPHY

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