CAT 3 - Paper Answers

CAT3 Supraventricular tachyarrhythmias

After completing your assigned readings (Chapter 132 in our Hospital Medicine text), can anyone answer the following questions about Supraventricular tachyarrhythmias?

What electrocardiographic findings help differentiate between the common SVTs?

What acute and chronic management strategies are indicated for various SVTs?

What comorbid conditions increase the risk of thromboembolic complications in patients with A-fib?

Which patients with A-fib deserve anticoagulation, and which of these patients need bridging anticoagulation until oral warfarin attains therapeutic INR?

Which SVTs deserve electrophysiologic intervention over medical management?

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CHAPTER 132
Supraventricular Tachyarrhythmias

Elbert B. Chun, MD

Gerard M. McGorisk, MD, FACC, MRCPI

Key Clinical Questions

What electrocardiographic findings help differentiate between the common
supraventricular tachyarrhythmias (SVTs)?

What acute and chronic management strategies are indicated for various SVTs?
What comorbid conditions increase the risk of thromboembolic complications in
patients with atrial fibrillation?

Which patients with atrial fibrillation deserve anticoagulation, and which of these
patients need bridging anticoagulation until oral warfarin attains therapeutic
international normalized ratio (INR)?

Which SVTs deserve electrophysiologic intervention over medical management?

EPIDEMIOLOGY

Supraventricular tachyarrhythmias (SVTs) comprise an array of narrow-complex
arrhythmias that originate above the ventricles and include both the most commonly

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encountered arrhythmia, atrial fibrillation (AF), and the uncommon ones, such as Wolfe-
Parkinson-White (WPW) syndrome. Based on Medicare and a sampling of national
community hospital discharge database, AF occurs 10-fold more frequently than
paroxysmal SVTs such as AVnRT. This chapter describes in detail the common atrial
arrhythmias encountered by hospitalists, and explains the uncommon arrhythmias that
hospitalists should recognize and manage with cardiologist or electrophysiologist
consultation or referral. The chapter will briefly describe arrhythmia mechanisms while
focusing on arrhythmia diagnosis, management options in the acute setting, and long-
term management strategies—all essential for a seamless transition beyond the inpatient
setting.

PRESENTATION
Common presenting symptoms of SVTs include rapid palpitations, chest discomfort,
dyspnea, presyncope, and syncope. Additionally, atrial fibrillation and atrial flutter may
present with new stroke symptoms. Particularly in the elderly with atrial fibrillation,
palpitations and chest discomfort are often absent and excessive fatigue is the
predominant symptom.

RISK STRATIFICATION

As SVT is a heterogenous disorder describing different arrhythmias with vastly different
clinical prognosis. As such, the crucial initial step is the proper recognition of the rhythm
disorder to individualize treatment strategy and prevention of adverse events.

RHYTHM IDENTIFICATION

When evaluating patients with a narrow-complex arrhythmia, the QRS complex is by
definition less than 120 ms. The regularity of the RR intervals then helps reduce the
numerous possibilities, as indicated in the SVT recognition algorithm (Figure 132-1). Only
four possibilities exist if the RR intervals are irregular: (1) atrial fibrillation, (2) atrial flutter
with variable atrioventricular (AV) node blockade, (3) atrial tachycardia with variable AV
node blockade, and (4) multifocal atrial tachycardia (MAT).

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Figure 132-1 Supraventricular tachyarrhythmia recognition algorithm. AF, atrial fibrillation;
Aflutter, atrial flutter; AT, atrial tachycardia; AV block, atrioventricular block; AVnRT,
atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentry tachycardia; MAT,
multifocal atrial tachycardia; PJRT, paroxysmal junctional reentrant tachycardia; SNRT,
sinus node reentry tachycardia.

More challenging to diagnose is the SVT with a regular RR interval. If, however, no P-
wave can be identified, this indicates the most common form of paroxysmal SVT:
atrioventricular nodal reentrant tachycardia (AVnRT). The P-wave in typical AVnRT is
buried within the QRS complex. If the P-wave is identified then determine if there is more
than one P-wave for each conducted QRS. If so, then only atrial flutter or atrial tachycardia
remains as possible diagnoses.

Finally, if only a one-to-one relationship between the P-waves and QRS complexes
exists, measuring the RP interval will further narrow the likely rhythms (Figure 132-2). The
response of the rhythm to bedside vagal maneuvers or intravenous adenosine can be used
to better differentiate the regular narrow-complex arrhythmias by transiently slowing the

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AV conduction and revealing the P-waves, converting the rhythm to sinus, or gradually
slowing and reaccelerating the tachycardia (Table 132-1).

Figure 132-2 ECG rhythm intervals demonstrating how to measure the PR and RP
intervals.

TABLE 132-1 Effect of Transient Atrioventricular Node Blockade on Supraventricular
Tachyarrhythmia Diagnosis

Rhythm
Response to Transient AV Node Blockade (Vagal
Maneuvers or IV Adenosine)

AVnRT Sudden termination
AVRT Sudden termination
Sinus reentry tachycardia Sudden termination
Focal atrial tachycardia Sudden termination, or gradual slowing and

reacceleration
Ventricular tachycardia (high
septal or fascicular origin)

No response

Sinus tachycardia

Gradual slowing, then reacceleration

Nonparoxysmal junctional
tachycardia

Gradual slowing, then reacceleration

Atrial flutter Persistent atrial tachycardia and transient high-grade
AV blockade

Macro reentrant atrial tachycardia Persistent atrial tachycardia and transient high-grade
AV blockade

AVnRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentry tachycardia;
VTACH, ventricular tachycardia.

Proceeding through the SVT recognition algorithm (see Figure 132-1) using a sample
ECG (Figure 132-3), the clinician first recognizes that the rate is greater than 100 beats per
minute (bpm). The QRS complexes are narrow, thus leading to a generic diagnosis of SVT.
Following the SVT recognition algorithm, the regularity of the RR intervals is assessed, and

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the absence of P-waves leads to the conclusion that the SVT is attributable to typical
AVnRT (see Figure 132-3).

Figure 132-3 Atrioventricular nodal tachycardia (AVnRT).

ATRIAL FIBRILLATION

EVALUATION

Before the age of 60, the prevalence of atrial fibrillation occurs uncommonly, in stark
contrast to the prevalence estimate of 8% among those older than 80 years. As AF is the
most common arrhythmia encountered by the inpatient clinician, this section will address
the questions pertaining to the valvular and nonvalvular etiology of this arrhythmia,
judicious utilization of cardioversion, thromboembolic and other complications, methods
for estimating risk of stroke, and management strategies in the acute and chronic settings.

Patients with atrial fibrillation are classified in one of three categories: (1) paroxysmal
AF, (2) persistent AF, or (3) permanent AF (Table 132-2).

TABLE 132-2 Atrial Fibrillation Nomenclature

Paroxysmal AF Episodes lasting <7 days and spontaneously converting to sinus rhythm

Persistent AF Episodes lasting >7 days unless chemical or
electrically cardioverted to sinus rhythm

Permanent AF AF resistant to multiple attempts at cardioversion
Lone AF AF in patients younger than 60 years old in the

absence of any predisposing factor

AF, atrial fibrillation.

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The atrium in patients with AF shows evidence of fibrosis and increased extracellular
mass changes that are seen both in the myocardium of the elderly and in ischemia-
induced hibernating myocardium. Within this scarred milieu, a focal-enhanced
automaticity and variance in atrial tissue refractory and conduction times (known
collectively as the multiple wavelet hypothesis) leads to this common arrhythmia. The
enhanced automaticity often can be isolated to atrial tissue near the pulmonary veins. In
addition to the aging process, any medical condition that leads to elevated left atrial
pressure and dilated atrium—hypertension, mitral stenosis or regurgitation, and any
cardiomyopathy—will predispose the patient to atrial fibrillation. Hyperadrenergic states—
sepsis, alcohol ingestion or withdrawal, postoperative state, and thyrotoxicosis—also
predispose to AF. Lone atrial fibrillation describes AF in patients younger than 60 years old
in the absence of any predisposing factor.

INPATIENT

MANAGEMENT

Hemodynamic compromise versus stable tachycardia

Common clinical scenarios for hospitalized patients with AF include those with stable
tachycardia and those with hemodynamic compromise. For those with hypotension, a trial
of short-acting rate-controlling agents (eg, esmolol) could be attempted to determine if
slowing the tachycardia may improve the hemodynamics, keeping in mind that these very
agents may exacerbate hypotension. Intravenous digoxin and amiodarone are options if
hypotension prevents the use of β-blockers and calcium channel blockers. Synchronized
direct cardioversion should be performed if the hypotension does not resolve (see Chapter
125). Currently there are two types of defibrillators: monophasic and biphasic. Biphasic
defibrillators are now significantly more common and require less energy and reduced
number of shocks delivered to achieve successful cardioversion. Biphasic defibrillators
also have reduced skin injury. The monophasic device should be set at a minimum of 200
J and a maximum of 400 J. The biphasic device demonstrates effective cardioversion at
200 J and often times at just 100 J for AF.

Rate control

One or multiple rate-controlling agents may be needed to provide adequate control of the
ventricular response (Table 132-3). After 24 hours on the intravenous infusion, switching
to an oral regimen can be initiated. β-Blockers and nondihydropyridine calcium channel
blockers are considered first-line agents. Intravenous digoxin and amiodarone are
reasonable options, particularly in the setting of congestive heart failure. An important
limitation of digoxin is that its vagally induced AV node blockade can be easily overcome
in nonsedentary patients. Although very effective in rate control and even rhythm
conversion, amiodarone has a long-term side effects profile which relegates its use as a
distant second option. Clinicians should target a heart rate under 110 bpm at rest but
consider patient symptoms in modification of rate control.

TABLE 132-3 Intravenous Medications for Rate-Control in Atrial Fibrillation or Atrial
Flutter

Medication Loading Dose
Maintenance
Dose Side Effects

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Esmolol 500 mcg/kg over 1 min 60-200
mcg/kg/min IV

Hypotension

Metoprolol 2.5-5 mg IV over 2 min
Up to 3 doses

NA Hypotension

Diltiazem 0.25 mg/kg IV over 2 min 5-15 mg/h Hypotension
Verapamil 0.075-0.15 mg/kg IV over

2 min
NA Hypotension

Digoxin 0.25 mg IV every 2 h up to
total dose 1.5 mg

0.125-0.375
mg/day IV or
orally

Digoxin toxicity, heart
block

Amiodarone 150 mg IV over 10 min 0.5-1 mg/min IV Pulmonary toxcity,
hepatitis, skin
discoloration, thyroid
dysfunction, corneal
deposits, optic
neuropathy

The presence of an accessory pathway would be an absolute contraindication in the
use of AV node-blocking agents. As electrical impulses are conducted nondecrementally
via the accessory pathway, the ventricular response in AF will actually increase and may
degenerate into ventricular fibrillation (VFIB).

Rhythm control and consultation

After assessing clinical stability and adequately controlling the rapid ventricular response,
the clinician should determine if the rhythm event is new, recurrent, or an exacerbation of a
permanent form of the arrhythmia. If the condition is a new event or a paroxysmal one
with infrequent yet very symptomatic recurrences and has been present for less than 48
hours, cardioversion—chemical or electrical—followed by an attempt to maintain a sinus
rhythm may offer symptom benefit and is recommended by the ACC-AHA AF guidelines
from 2006 (Table 132-4). If the AF duration is longer than 48 hours, cardioversion remains
an option after transesophageal echo (TEE) is negative for left atrial thrombus.
Cardioverting those with new-onset AF provides the theoretical benefit of curtailing the risk
of developing permanent AF.

TABLE 132-4 Indication for R-Wave Synchronized Cardioversion in Atrial Fibrillation

Rapid ventricular response not responding to pharmacologic measures in setting of
ongoing angina, heart failure, myocardial ischemia, or symptomatic hypotension
Pre-excitation with rapid ventricular response or hemodynamic instability
Stable hemodynamics, but poorly tolerated symptoms
Early relapse of atrial fibrillation after attempted cardioversion, proceed with
administration of antiarrhythmic medications first, then repeat cardioversion
Consider patient preferences in the setting of infrequent relapses

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Cardioversion can be achieved not only with electrical means, but also chemical
means (Table 132-5). The antiarrhythmics used for cardioversion should be considered
after consultation with cardiology service. A class III agent, ibutilide, can be used in select
patients that have no evidence of systolic dysfunction, normal magnesium and potassium
levels, and a normal corrected QT interval (QTc). Due to the risk of torsades de pointes,
this should be performed in a setting equipped to handle this potential complication.
Ibutilide has the advantage of increasing the success of electrical cardioversion following
a failed chemical cardioversion. An oral class III agent, tikosyn, can be used to both
convert to a sinus rhythm and also maintain a sinus rhythm. This medication should be
reserved for cardiology consultants due to the need for close monitoring of the QT interval,
renal dose adjustments, and limitations of use in patients with liver dysfunction. If the QT
interval is greater than 500 ms, this medication should not be initiated or should be
discontinued. The use of medications to maintain a sinus rhythm should remain under the
care of a cardiologist due to the frequency of treatment failure and significant risk of
malignant ventricular arrhythmias.

TABLE 132-5 Medications for Pharmacologic Cardioversion of Atrial Fibrillation

Medication
Antiarrhythmic
Class Dosing Route Comments

Amiodarone
(codarone,
pacerone)

III 400 mg orally twice a
day for 2 wks (10 g
load), then 200 mg
orally every day
150 mg IV over 10
mins, then 1 mg/min
for 6 h, then 0.5
mg/min for 18 h (1 g
load)

Orally Outpatient option: oral
load (gastrointestinal
side effects common)
Other side effects
common and severe:
pulmonary fibrosis,
corneal deposits,
thyroid dysfunction,
hepatitis, skin
deposition

Ibutilide
(corvert)

III If weight >60 kg, 1 mg
IV once; may repeat
dose if no response in
10 mins
If weight <60 kg, then 0.01 mg/kg IV; may repeat if no response after 10 mins

IV Inpatient only usually
cardioverts within 1 h
monitor for QT
prolongation
Torsades 4% (more
common in women)
Must monitor K+ and
Mg+2

Dofetilide
(tikosyn)

III 500 mcg orally twice
a day (restricted
distribution in the US
to trained prescribers
and facilities)

Orally Inpatient initiation only;
adjust for renal
function, age, body size
QT prolongation

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Many drug interactions
(CYP3A4)
Contraindicated with
Bactrim, HCTZ,
verapamil

Flecainide Ic Start 50 mg orally
twice a day, may
increase 100 mg/d
every 4 days; max
dose 300 mg every
day

Orally
or IV

Contraindicated in
structural heart disease
Adjust dose for renal
dysfunction

Propafenone Ia Start 150 mg orally
three times a day, then
may increase to 225
mg orally three times
a day after 4 days,
then, up to 300 mg
orally three times a
day

Orally
or IV

Contraindicated in
structural heart disease
including significant
LVH, CHF, severe
obstructive lung
disease

Anticoagulation

The unorganized atrial contractions during AF will lead to the formation of thrombus or
spontaneous echo contrast (SEC) within the left atrium or the left atrial appendage posing
a substantial risk of thromboembolic phenomena to the arterial circulation, which usually
manifests as stroke and, less commonly, mesenteric ischemia or an acutely ischemic limb.
The transthoracic echocardiogram is considered the diagnostic test of choice for initial
evaluation. It is useful in assessing left atrial size and left ventricular function, but cannot
exclude atrial thrombus. The transesophageal echocardiogram provides high resolution of
the left atrium and left atrial appendage and to exclude thrombus and permit early
cardioversion. Thrombus or dense SEC would preclude the option for early cardioversion
and necessitate the need for full anticoagulation for 4 weeks prior to cardioversion. In the
absence of thrombus or SEC on TEE, the patient may receive early cardioversion in the
setting of anticoagulation. For AF recognized greater than 48 hours after onset in patients
who do not undergo TEE, full anticoagulation for 4 weeks is recommended followed by
cardioversion, if indicated.

In either strategy, anticoagulation for a minimum of 4 weeks postcardioversion is
necessary to reduce the risk of thromboembolic complications. The risk of embolic stroke
is approximately 1% with either approach. Stroke risk postcardioversion is due to a
“stunning” effect on the left atrium after any form of cardioversion (electrical, chemical, or
even spontaneous). This stunning refers to a delay in the resumption of mechanical
contraction of the left atrium, providing an environment ripe for stasis and thrombus
formation. Benefits from an early cardioversion approach include quicker conversion to a
sinus rhythm, accelerated care for the patient, and potentially less bleeding complications
associated without the preceding 4 weeks of anticoagulation.

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PRACTICE POINT

Transesophageal echocardiogram is a highly sensitive test to rule out thrombus within
the left atrium and left atrial appendage to permit an early cardioversion strategy, if
indicated.

Ablation strategies

Invasive management options for atrial fibrillation should be considered secondary
options following failure of medical therapies and recurrent admissions due to
symptomatic palpitations or heart failure exacerbations. The palpitations associated with
atrial fibrillation can be distressing to some individuals, particularly younger patients, and
have significant negative impacts on quality of life. If the use of antiarrhythmic regimens
has failed, options for catheter-based interventions or even intraoperative left atrial
ablation, also known as the Maze procedure can be offered. One catheter-based approach
called ablate-and-pace, entails ablating the AV node and then pacing the ventricle. Another
catheter-based approach involves isolating the focus of automaticity, usually near the
pulmonary veins of the cavoatrial isthmus, ablating the foci, and initiating anticoagulation
therapy thereafter. The latter approach is relatively new and long-term outcome research is
still pending. The short-term safety of the procedure in centers with established experience
has been proven with death rates or stroke rates under 1% and overall major
complications about 6% based on international survey data. However, the mean age of the
patients enrolled in these trials was 55 years old with intact systolic function and relatively
nondilated atrial diameters. More long-term outcome data will be needed before catheter-
based interventions can be considered a parallel option to medical treatment. A final
option usually reserved for those who are undergoing open heart bypass or valve
replacement is the Maze procedure, and even left atrial appendage resection, both of
which may prevent the occurrence of postoperative atrial fibrillation.

Death or significant neurologic deficits occur in 71% of patients with their first episode
of embolic complications associated with AF. Reducing this risk is a crucial component in
the management of AF. The annual risk of strokes for AF is approximately 4.5% per year,
which is reduced by two-thirds (to 1.5% per year) if patients are fully anticoagulated.
However, not all patients with this condition carry the same risk of embolic events and,
therefore, should be managed based on risk. Clinicians must diagnose the etiology of AF,
as that will help determine risk and direct management. The vast majority of AF is
nonvalvular, but valvular etiologies such as significant mitral stenosis must be considered.
A severalfold increase in thromboembolic risk occurs with mitral valve stenosis-associated
atrial fibrillation, and mandates full anticoagulation regardless of other stroke risk factors
present. Patients with other risk factors leading to atrial fibrillation have variable levels of
evidence supporting full anticoagulation, and some patients with few stroke or embolism
risk factors may not attain benefit from anticoagulation that outweighs its risks (Table
132-6).

TABLE 132-6 Antithrombotic Recommendations for Atrial Fibrillation by Etiology

AF Risk Factor Therapy Recommendation Level of Evidence

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Thyrotoxicosis Full anticoagulation (eg,
warfarin)

Level C: Expert opinion
(ACC/AHA guidelines)

Mitral stenosis Full anticoagulation (eg,
warfarin)

Level C: Expert opinion
(ACC/AHA guidelines)

Mechanical valve Full anticoagulation (eg,
warfarin)

Level 1A (ACCP guidelines
2008)

CHADS2 score ≥ 2 Full anticoagulation (eg,
warfarin)

Level 1A (ACCP guidelines
2008)

CHADS2 score = 1 Full anticoagulation (eg,
warfarin) or aspirin (75-325
mg daily)

Level 1A (anticoagulation)
Level 1B (asprin)
(ACCP guidelines 2008)

CHADS2 score = 0 Aspirin therapy (75-325 mg
daily)

Level 1B
(ACCP guidelines 2008)

ACC/AHA, American College of Cardiology/American Heart Association; ACCP, American College of
Chest Physicians.
Level 1A (ACCP): Consistent evidence from randomized controlled trials without important limitations
or exceptionally strong evidence from observational studies.
Level 1B (ACCP): Evidence from randomized controlled trials with important limitations (inconsistent
results, methodologic flaws, indirect or imprecise), or very strong evidence from observational studies.
Level C (ACC/AHA): Recommendation based on expert opinion, case studies, or standards of care.

When considering the more common scenario of nonvalvular atrial fibrillation, multiple
risk stratification strategies have been published over the decades to estimate the risk of
thromboembolic complications, and to date the one most widely used and derived from
large cohort data is known as the CHADS2 score. Congestive heart failure, Hypertension,
Age ≥ 75, and Diabetes each contributes one point in this risk stratification tool whereas
Stroke contributes two points. The total number of points corresponds to a level of risk
(incidence) of embolic stroke each year (Table 132-7).

TABLE 132-7 CHADS2 Score and Stroke Risk

Number of Factors Risk of Stroke (%/y)
0 (lower risk) 1.9 (1.2-3.0)
1 (intermediate risk) 2.8 (2.0-3.8)
2 (high risk) 4.0 (3.1-5.1)
3 5.9 (4.6-7.3)
4 8.5 (6.3-11.1)
5 12.5 (8.2-17.5)
6 18.2 (10.5-27.4)

CHADS2 score is calculated by adding 1 point for each of the following:

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Recent Congestive heart failure, Hypertension, Age ≥75 years, Diabetes mellitus; and 2 points for prior
Stroke/transient ischemic attack.

By using this risk stratification tool clinicians can balance the benefits of therapeutic
anticoagulation against the well-known complication, bleeding. With no risk factors for
thromboembolic phenomena, as in the scenario of lone atrial fibrillation, the risk of
bleeding complications with coumadin outweighs the benefit of stroke prevention. An
acceptable alternative stroke risk-reduction strategy for patients who have low baseline
risk (CHADS2 = 0) or who have contraindications to anticoagulation is antiplatelet therapy
with aspirin (81-325 mg daily).

For patients with intermediate risk (CHADS2 score = 1), one should implement an
additional risk stratification tool known as the CHA2DS2-VASc (Table 132-8) to better
define the risk of thromboembolic stroke. As recommended by national cardiology
organizations, anticoagulation should be strongly considered if the score is 2 or greater. If
the score 1 point, then either aspirin or anticoagulation are viable options. Major bleeding
complication risk with anticoagulation can be estimated using a risk stratification scheme
with the acronym HAS-BLED (Table 132-9).

TABLE 132-8 CHA2DS2-VASc

Number of Factors Risk of stroke (%/y)
0 0
1 1.3
2 2.2
3 3.2
4 4.0
5 6.7
6 9.8
7 9.6
8 6.7
9 15.2

CHA2DS2-VASc score is calculated by adding 1 point for each of the following: Recent CHF,
hypertension, Age 65-74, DM, female gender, Vascular disease (PVD, CAD, aortic plaque); and 2 points
for Age ≥75 and prior Stroke/TIA.

TABLE 132-9 HAS-BLED Score

Letter Clinical Characteristic Points
H Hypertension 1
A Abnormal renal or liver disease 1 for each
S Stroke 1

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B Previous major bleeding 1
L Labile INR 1
E Elderly (age >65) 1
D Drugs or alcohol 1

Hypertension – SBP >160 mm Hg
Abnormal renal function: dialysis or serum creatinine >2.26 mg/dL (200 umol/L)
Abnormal liver function: cirrhosis, or elevated AST or ALT >3 X upper limit of normal
Labile INR: unstable INR or TTR (time in therapeutic range) <60% Drugs: aspirin, other antiplatelet medications, NSAIDS, or alcohol abuse

The HAS-BLED score contains the variables hypertension, abnormal renal function,
abnormal liver function, stroke, previous bleeding, labile INR’s, age >65 years old,
concomitant use of aspirin or antiplatelet agent, and excessive alcohol consumption with
each counting as a point. The final score then correlates with the risk of major bleeding
per 100 patients per year (ie, % major bleeds per year with anticoagulation therapy).

These risk estimation tools can be used to counsel patients regarding treatment
choices, including benefits and risks, and help identify patients who might gain more
overall benefit from antiplatelet aspirin therapy rather than anticoagulation. The HAS-
BLED tool might also be used to help determine which patients deserve more intensive
outpatient monitoring of their anticoagulation (eg, in an anticoagulation clinic). National
organizations recommend using caution when the HAS-BLED score ≥ 3 and a detailed
discussion of risk and benefits with the patient.

More data over the past several years have demonstrated a larger role of AF in patients
with cryptogenic strokes. Insertable cardiac monitors in a study published in 2015 have
been utilized in this cohort of patients and have detected up to 8.9% patients with AF at 6
months compared to just over 1% in the cohort following standard of care monitoring. The
most recent national medical organizations do not provide strong guidance in the intensity
and duration of monitoring for potential AF detection in cryptogenic, but this data
suggests a 24-hour Holter monitor is vastly insufficient.

ATRIAL FIBRILLATION AND OLDER PEOPLE: WARFARIN CONTROVERSY

Often a difficult clinical management decision, the use of anticoagulation in older patients
is controversial. Atrial fibrillation is the etiologic factor for 36% of strokes in individuals
over the age of 80. The morbidity and mortality of a first stroke due to this disease is 71%.
Meta-analysis data estimate the overall risk reduction with vitamin-K antagonists at 66%
and with aspirin at 21%. Recent data have also demonstrated that patients over the age of
85 benefit more from anticoagulation than younger cohorts. Thus, the argument for
anticoagulation with warfarin in this group is compelling. However, the risk of major
bleeding complications is still relevant. The rate of intracranial hemorrhage (ICH) while
taking warfarin is approximately 0.3% to 0.6% per year (RR ~ 2, compared to control).
Aspirin also carries an increased risk of ICH (RR ~ 1.4 compared to control). Although the
risk of ICH seems low, this estimate may be underestimated as older patients were
underrepresented in the early randomized trials performed almost 20 years ago. More

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recent observational studies have estimated the risk of a major bleeding complication in
individuals over the age of 80 to be 13% per year including a 2.4% per year risk of ICH.

Additional concerns for anticoagulation in older people are the increased risk for falls,
likely drug interactions due to polypharmacy, complexity of coumadin regimens, need for
close monitoring, and the large representation of nursing home patients. Even in research
trials studying the efficacy of coumadin to prevent strokes, only two-thirds of the INRs
were in the therapeutic range. Some of these concerns can be addressed with the novel
oral anticoagulants that reduce the need for frequent laboratory monitoring and reduce the
concerns for drug interactions associated with polypharmacy. The data comparing
coumadin with the direct thrombin inhibitor, dabigatran, demonstrate better stroke
prevention with the higher dose of dabigatran at 150 mg orally twice a day and even a
trend toward an overall mortality benefit after a median follow-up period of 2 years. The
downside is the increased propensity of gastrointestinal bleeding compared to warfarin.
The lower dose, 110 mg orally twice a day, was found to have an equivalent reduction of
stroke risk and a lower risk of major bleeding complications but is not available in the
United States. There are also three factor Xa inhibitors that Food and Drug Administration
(FDA) approved to prevent strokes in the setting of nonvalvular AFIB, rivaroxaban,
apixaban, and edoxaban. Rivaroxaban has been shown to be noninferior in stroke
prevention, major bleeding complications, and mortality with warfarin. Apixaban however
has been shown to prevent slightly more strokes, reduce risk of major bleeding outcomes,
and reduce risk for mortality compared to warfarin. The most recent FDA approval of
edoxaban in January 2015 was based on randomized trial data demonstrating superior
stroke prevention compared to warfarin, less major bleeding complications, but slightly
higher gastrointestinal bleeding complications. All of the novel anticoagulants compared
to Coumadin have half as many intracranial bleeds. As no head-to-head studies have been
conducted among the novel agents, all are considered viable options for stroke prevention
for nonvaluvular AFIB.

PRACTICE POINT

Novel anticoagulants reduce the need for frequent laboratory monitoring and reduce
the concerns for drug interactions associated with warfarin and polypharmacy. These
medications (dabigatran, rivaroxaban, apixiban, edoxaban) are approved for use in
atrial fibrillation for stroke prevention. However, the cost may be prohibitive if not
insured.
Apixiban received FDA approval in 2015 for use in patients with ESRD on
hemodialysis despite the absence of randomized control data but supported by
pharmacokinetic data.
Risk scores such as CHADS2, CHA2DS2-VASc apply only to nonvalvular AFIB. AFIB
related to mechanical valves, mitral stenosis or rarely hyperthyroidism are at much
higher risk for thromboembolic phenomena and require anticoagulation.
The novel anticoagulants have not been FDA approved in patients with mechanical
heart valves. In fact, dabigatran has been shown to have been inferior to coumadin in
preventing embolic stokes with mechanical heart valves.
The ACCP 2012 guideline on antithrombotics recommends the use of bridging
anticoagulation in AF in high risk patients with a CHADS2 score of 5 and 6. This has

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been supported by 2015 randomized trial BRIDGE which demonstrated more bleeding
complications and no change in stroke prevention in those undergoing a bridging
strategy.
Bridging anticoagulation for those with low or moderate risk AFIB increases the risk of
major bleeding complications and has not been proven to prevent more
thromboembolic events via recent observational data and large randomized control
trial in 2015.

Randomized trial data for the use of other antiplatelet agents (clopidogrel) in addition
to aspirin for stroke prevention has been equivocal with respect to outcomes, with modest
risk reduction of stroke but similar risk increase for major bleeding complications. Dual
antiplatelet agents for stroke prevention are, therefore, not currently recommended.

POSTOPERATIVE ATRIAL FIBRILLATION

Postoperative atrial fibrillation (POAF) is the most common arrhythmia after surgery and
observational data suggest an increased risk of short- and long-term mortality, increased
length of stay, hospital costs, ICU length of stay, and stroke risk with this arrhythmia.
Recent observational data in 2014 strongly suggest a twofold increase in stroke risk in
patients with POAF compared to those with who didn’t develop AF after noncardiac
surgery at 1 year. This was also true in those who underwent cardiac surgery but to a
lesser degree (hazard ratio 1.3, CI 1.1, 1.6). POAF is also the most common reason for
hospital readmission after open heart surgery. The risk of developing this arrhythmia
varies based on the type of surgical intervention, with open heart procedures bearing the
highest risk (Table 132-10). Some of the risk factors associated with POAF include age,
atrial enlargement, procedures related to the heart such as valvular repair, and β-blocker
discontinuation.

TABLE 132-10 Risk of Postoperative Atrial Fibrillation (POAF) Based on Type of Surgery

Surgery Type POAF/SVT %
Thoracic (noncardiac) 9-29%
Cardiothoracic 20-40%
Orthopedics 4%

The peak incidence of POAF occurs on the second postoperative day, and the majority
occurs within 5 days postoperative. The majority of recurrent episodes of POAF occurred
within several days of the first episode. The majority of POAF rhythms will spontaneously
revert to sinus rhythm by the sixth postoperative week. However, if POAF is poorly
tolerated due to hemodynamic compromise, anticoagulation and cardioversion would be
recommended. Preoperative β-blockade leads to significant reduction in POAF incidence,
but conflicting data mire the actual effect on hospital length of stay, postoperative strokes,
and mortality. The ACC/AHA 2006 guidelines for AF offer a class I recommendation of
perioperative β-blockers for prevention of POAF in patients undergoing coronary
revascularization surgery (CABG).

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POSTACUTE CARE: ATRIAL FIBRILLATION

If a patient is discharged on warfarin, rapid follow-up within 3 to 5 days is warranted as
the risk of major bleeding complications is known to occur with initiation of
anticoagulation. If an anticoagulation clinic is available, it would be strongly
recommended to be monitored there. Within a week or two, the heart rate response can be
reassessed as most patients will require AV nodal blocking agents to prevent a rapid
ventricular response. The patient’s symptoms can be periodically reassessed to determine
whether the treatment strategy, either rate-control or rhythm control, needs to be changed.
It should be noted that the latter approach has not been proven to reduce mortality, but
only to improve symptoms and quality of life for a select group a patients with intolerable
palpations and fatigue associated with AFIB.

DISCHARGE CHECKLIST: AFIB

Transthoracic echocardiogram should have been performed recently to differentiate
between valvular and nonvalvular AFIB and assess ventricular function and left
atrial size.
Thyroid function tests should have been completed to evaluate for hyperthyroidism.
For new onset AFIB, early consultation with cardiology should be considered to
evaluate the potential benefits of a rhythm control strategy.
Ensure stroke risk stratification with CHADS2 or CHA2DS2-VASc has been discussed
with the nonvalvular AFIB patient and documented.
Ensure risk stratification for major bleeding complications via HAS-BLED has been
discussed with patients on anticoagulation.

For those on vitamin-K antagonists, rapid follow-up within 3 to 5 days should
occur to avoid the perils of major bleeding complications.
For those on novel anticoagulants, ensure dosing has been based on level of renal
function as FDA-approved antidotes are not available for the factor Xa inhibitors.
For those with cryptogenic stroke, strongly consider longer-term monitoring via an
event monitor or insertable cardiac monitor to sufficiently evaluate for potential
unrecognized AF.

ATRIAL FLUTTER

EPIDEMIOLOGY

Atrial flutter is the next most common form of SVT after atrial fibrillation and can manifest
into the typical and atypical pattern. The typical pattern, also known as counterclockwise
flutter due to the pattern of the macro reentry electrophysiologic mechanism, manifests as
a sawtooth pattern, typical for the P-wave negative deflections (Figure 132-4). The second
form of atrial flutter has the opposite pattern with positive deflections in the P-wave
sawtooth pattern (Figure 132-5). Even though the atrial rate ranges from 240 to 300
beats/min, the AV nodal block will prevent all the atrial impulses from reaching the
ventricle. The block at the AV node is frequently 2:1 but can also manifest as 3:1 and 4:1
or even variable block. The individuals that develop atrial flutter usually have a disorder
that directly or indirectly involves the right atrium. Tricuspid valvular disease, various

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pulmonary disorders, postsurgical repair of congenital heart disease, or any process
leading to the enlargement of the right atrium increase the risk for atrial flutter.

Figure 132-4 Atrial flutter (2:1 block) with typical negative deflection P-waves revealing
the classic “sawtooth” pattern.

Figure 132-5 Atrial flutter (2:1 block) with positive deflection P-waves revealing an upward
“sawtooth” pattern.

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PRACTICE POINT

Any disease process leading to the enlargement of the right atrium increases the risk
for atrial flutter.

EVALUATION

Practice guidelines from national and international organizations recommend to approach
atrial flutter in the same manner as atrial fibrillation. A priority should be to ensure
hemodynamic stability in the setting of a rapid ventricular rate and use of early
anticoagulation barring contraindications. An echocardiogram will evaluate for any
potential structural heart disease and clinical evaluation for any medical condition leading
to increased right-sided heart disease.

MANAGEMENT

The management of atrial flutter is similar to the management of atrial fibrillation.
Ventricular rate control is achieved by increasing the block at the level of the AV node to
reduce ventricular response to the rapid atrial rate. Certainly if the patient is
hemodynamically compromised, direct cardioversion should be performed (biphasic 100
J, monophasic 200 J). In contrast to AF, using calcium channel blockers or β-blockers
alone are frequently insufficient in rate controlling the rhythm. It is often necessary to
consider the addition of a class Ic antiarrhythmic, such as flecanide, to achieve
satisfactory results. The class I agents are able to suppress the frequency of premature
atrial beats, which trigger the development of this arrhythmia. Other agents to consider
would be class III agents such as ibutilide for chemical cardioversion. Sotalol and
amiodarone may also be used, but side effects need to be considered in chronic
management.

PRACTICE POINT

In atrial flutter, avoid using flecainide as the sole treatment due to its ability to
decrease the reentry circuit cycle length and potentially induce a fast, unstable 1:1
ventricular response and subsequent degeneration into ventricular fibrillation.

The risk of thromboembolic complications in atrial flutter is thought to be similar to
that of atrial fibrillation, although there is a relative paucity of data compared with AF. For
these patients, full anticoagulation should be strongly considered. Additionally,
approximately 75% patients with atrial flutter also develop atrial fibrillation.

In contrast to atrial fibrillation, catheter-based intervention should be considered early
in atrial flutter with rapid ventricular rate as medical therapy is frequently suboptimal.
Success rates approaching 90% are reported with radiofrequency ablation (RFA) of the
cavotricuspid isthmus, leading to a bidirectional block inhibiting the macro reentry
mechanism of flutter. Due to the remaining anatomic or electrophysiologic conditions that
remain after the RFA, the procedure is not considered curative. The recurrence rate is 10%
to 20% over a period of 2 years but compares very favorably to the 60% recurrence rate of

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medical treatment alone. Less-frequent hospitalizations, lack of concern for medication
side effects, and improved sense of quality of life are other factors weighing favorably
toward a catheter-based ablative approach to atrial flutter management.

PRACTICE POINT

A strong consideration of catheter-ablation strategy should be considered in patients
with atrial flutter and rapid ventricular rate as medical management of rapid
ventricular rate is frequently suboptimal.

ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA
EPIDEMIOLOGY

Atrioventricular nodal reentrant tachycardia (AVnRT) is the most common form of
paroxysmal SVT, responsible for almost two-thirds of episodes; it is estimated that 10% of
the general population has AVnRT. The palpitations characteristically start abruptly and
may last for just a few minutes to as long as a few hours. They terminate as abruptly as
they start. Additional symptoms include chest discomfort, dyspnea, lightheadedness, neck
pulsations, and associated anxiety. These symptoms are often misdiagnosed as panic
attacks if the arrhythmia is not caught while on a monitor. Signs of the arrhythmia include
regular tachycardia with a heart rate between 120 and 200 bpm. Vagal maneuvers such as
carotid sinus massage or the Valsalva maneuver can break the reentry circuit. This
arrhythmia is usually not associated with structural heart disease and carries very little
risk of death.

The mechanism of this tachyarrhythmia is a reentry circuit composed of the atrium, AV
node or perinodal tissue, and the ventricle. The perinodal tissue or AV node exhibits a dual
c

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proved sense of quality of life are other factors weighing favorably toward a catheter-
based ablative approach to atrial flutter management.

PRACTICE POINT

ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA
EPIDEMIOLOGY

The mechanism of this tachyarrhythmia is a reentry circuit composed of the atrium, AV
node or perinodal tissue, and the ventricle. The perinodal tissue or AV node exhibits a dual
conduction physiology that reveals a slow pathway with an inherently short refractory
period and a fast pathway with a relatively long refractory period.

There are three variants of AVnRT that depend on the routes of conduction.
Approximately 90% of AVnRT is called typical AVnRT based on its antegrade conduction
via the slow pathway and retrograde conduction via the fast pathway. With this typical
conduction the surface ECG has the characteristic P-waves either buried within the QRS
complex or just after the QRS. As expected with fast retrograde conduction, the RP interval
is shorter than the PR interval. Recognizing the relative length of the RP and PR intervals
can further differentiate between the other SVTs. The ECG for the typical AVnRT often
demonstrates a pseudo-R’-wave in V1 and pseudo-S’-waves in inferior limb leads. The less
common variants include fast/slow and slow/slow, which will demonstrate clear P-waves,
inverted in the inferior limb leads with an RP interval longer than the PR interval.

MANAGEMENT

Initial hospital management

Management of AVnRT can follow a straightforward treatment sequence (Figure 132-6).
Vagal maneuvers such as the carotid sinus massage and Valsalva maneuver can break

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the reentry circuit 25% of the time. If the tachycardia is refractory to these maneuvers,
adenosine will convert the rhythm to sinus in approximately 90% of patients. Due to its
very short half-life of less than 10 seconds, it is crucial that adenosine be given as a rapid
bolus and immediately followed by 5 to 10 mL of saline. Adenosine is typically dosed in 6
mg increments, but patients usually respond to a 12-mg dose. The expected symptoms
with the infusion are dyspnea, facial flushing, and chest discomfort that last under a
minute. When using adenosine, the patient’s rhythm should be monitored by telemetry via
a continuously running 12-lead ECG to observe the response that occurs within 30
seconds.

Figure 132-6 Treatment sequence for atrioventricular nodal reentrant tachycardia (AVnRT).

PRACTICE POINT

AVnRT can be converted to sinus rhythm with vagal maneuvers in 25% of cases and
with adenosine in 90% of cases. Adenosine must be given as a rapid IV bolus and
immediately followed by 5-10 mL of saline. The expected symptoms with the infusion
are dyspnea, facial flushing, and chest discomfort that last under a minute. When
using adenosine, the patient’s rhythm should be monitored continuously with

rhythm

strip or 12-lead ECG to monitor the response, which occurs within 30 seconds.
Recent randomized data demonstrated in 2015 that a “modified Valsalva maneuver”
converted 40% of patients with SVT compared to just 17% of those who underwent the
standard Valsalva maneuver. The steps to this modified maneuver is as follows:
a. semirecumbent position—head of bed at 45° angle
b. have patient blow into a 10-cc syringe for ~15 seconds with enough pressure to just

move the plunger
c. then, immediately lay patient in the supine position and raise the legs up to ~45°

Typically, adenosine will convert the AVnRT to a sinus rhythm, but other possible
rhythms include ventricular ectopy, transient sinus pause, transient bradyarrhythmias,
atrial fibrillation or atrial flutter uncommonly, and, very rarely, polymorphic ventricular
tachycardia. The risk of torsades de pointes is increased in patients with a baseline
prolonged QTc. Factors that could decrease the efficacy of intravenous adenosine push
include the use of methylxanthine products such as theophylline and caffeine, which
block the A1 receptors. The use of dipyridamole (persantine, aggrenox) can augment the
efficacy of adenosine by slowing its clearance. Due to the potential for exacerbating
bronchospams, asthma is a relative contraindication for adenosine use. The transplanted

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heart is hypersensitive to adenosine, therefore a reduced dose or abandoning this
approach altogether is appropriate in such patients.

Other options beside adenosine for the acute management of AVnRT include
verapamil, β-blockers, and direct cardioversion. Verapamil, a nondihydropyridine calcium
channel blocker, will block both fast and slow pathways. Dosing for acute management is
5 mg IV every 10 minutes and has been reportedly 90% effective. The downside to
verapamil is the potential for hypotension that could be severe and long lasting. Another
option includes digoxin, although this approach is not optimal due to its delayed effect.
Direct cardioversion with 10 to 50 J is a final option if the previous interventions prove
ineffective.

Outpatient longitudinal therapeutics

If the patient has frequent episodes that negatively impact quality of life, the use of
invasive catheter ablation may be considered. The consensus approach by the ACC/AHA
guidelines recommends ablation of the slow pathway due to its high efficacy (97%) and
low risk of high-grade AV block (1%). The patient does need to consider the possibility of
pacemaker placement if high-degree block develops as a complication. Long-term medical
management is another option and includes medications such as verapamil, propanolol or
class I antiarrhythmic agents such as flecanide and propafenone. The medications can be
used on a daily basis to reduce the frequency of occurrences and the length of episodes.
Additionally, the “pill-in-the-pocket” method obviates the daily use and could be used just
during the episode. Cardiology consultation is indicated when using class I
antiarrhythmics due to the risk of malignant ventricular arrhythmias.

ATRIOVENTRICULAR REENTRY TACHYCARDIA

EVALUATION

The next most common form of a paroxysmal SVT is atrioventricular reentry tachycardia
(AVRT), which is characterized by an accessory conduction pathway between the atrium
and ventricle that serves as a conduit for macro reentry. This pathway is a muscular
bundle with variable properties of conduction, sometimes with bidirectional properties and
in others just unidirectional capabilities. A commonly cited example of AVRT is Wolf-
Parkinson-White syndrome, a narrow-complex tachyarrhythmia that manifests
symptomatically with palpitations, chest discomfort, dyspnea, presyncope or syncope,
and, very rarely, sudden cardiac death.

A baseline ECG when in sinus rhythm may (“revealed”) or may not (“concealed”)
demonstrate the delta wave (Figure 132-7). The accessory pathway depolarizes the
ventricular myocardium before the normal conduction system and is thus considered “pre-
excitation.” On the ECG, this will appear as the short PR interval. Due to the relatively
inefficient conduction from myocardial to myocardial cell (in contrast to the efficient His-
Purkinje system), the initial portion of the QRS is slurred (delta wave) and gives the QRS a
widened appearance (Figure 132-7). This accessory pathway, known as the bundle of Kent
in WPW syndrome, provides the electrical wave front a conduit to move from the ventricle
to the atrium, completing the macro reentry circuit.

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Figure 132-7 Atrioventricular reentry tachycardia (AVRT). Wolf-Parkinson-White (WPW)
syndrome with characteristic short PR interval and delta wave best seen in I, aVL, V3, and
V4.

INPATIENT MANAGEMENT

Management of this macro reentry arrhythmia is identical to the management for nodal
reentry tachycardia with vagal maneuvers as a first option and intravenous adenosine
push if unsuccessful. As discussed previously, adenosine administration usually converts
the rhythm to sinus; however, less frequently atrial fibrillation or atrial flutter can develop.
In very rare situations, the electrical impulse could conduct antegrade via the accessory
pathway, leading to a very rapid ventricular rate, ventricular instability, and polymorphic
ventricular tachycardia. This very rare complication of adenosine in AVRT requires having
a crash-cart available during adenosine administration.

In some types of AVRT, the accessory pathway may not be recognizable on the ECG
(considered concealed). When the accessory pathway conducts unidirectionally only from
the ventricle to the atrium, the characteristic delta wave, short PR interval, and widened
QRS are absent. The management remains the same as in the revealed WPW syndrome
with very little concern for polymorphic ventricular tachycardia, as the accessory pathway
will only conduct unidirectionally in a retrograde fashion from the ventricle to the atrium.

Beyond the acute management of AVRT, the frequency and severity of the palpitations
will guide long-term treatments. Infrequent episodes that are short in duration and
hemodynamically tolerable require only rest and time to resolve. A pill-in-the-pocket
regimen could be considered with class Ia, Ic, or III antiarrhythmics or AV nodal-blocking
agents as an option in this scenario in the absence of pre-excitation. However, if the
episodes are frequent and prolonged, daily use of these medications can be considered.
These antiarrhythmics will prolong the refractory period for both the accessory pathway
and the AV node, effectively preventing the arrhythmia or breaking the circuit during the
episodes. Radiofrequency ablation of the accessory pathway provides another option

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(with a very high success rate and low complication rate) for permanent rhythm control
that obviates the need for chronic medication in AVRT.

PRACTICE POINT

Wolf-Parkinson-White with atrial fibrillation:
Atrial fibrillation (AF) in a very young patient should lower clinicians’ threshold to
consider WPW syndrome. AF occurs in up to one-third of patients with WPW and is the
root cause for sudden death in these patients.
The patient with a “revealed” WPW and atrial fibrillation will demonstrate a wide QRS
complex on ECG due to the delta wave (often misinterpreted as atrial fibrillation with
bundle branch block, BBB).
WPW with AF should not be rate controlled with AV node-blocking agents, as atrial
impulses would be forced to the incrementally conducting accessory pathway. The
ventricular response would become 1:1, leading to unstable ventricular tachycardia
(see Figures 132-8 and 132-9).

Figure 132-8 Atrial fibrillation with brief run of aberrant conduction and noticeably wider
conduction in the latter half of the ECG strip.

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Figure 132-9 Unstable ventricular tachycardia after patient was given IV adenosine. This
AV nodal-blocking agent effectively shunted the atrial electrical impulses to the accessory
pathway, which is characterized by nondecremental conduction.

Treatment: IV procainamide or IV amiodarone or electrical cardioversion.

The presence of a delta wave on a resting ECG does not require a cardiology
consultation. However, a delta wave with a history of palpitations, syncope, or presyncope,
or with a history of atrial fibrillation does require cardiology consultation. The
electrophysiologist can perform invasive procedures to stratify some patients with the
WPW syndrome for risk of sudden cardiac death, especially when the refractory period for
the accessory pathway is short (RR interval of < 250 ms).

MULTIFOCAL ATRIAL TACHYCARDIA

EVALUATION

Multifocal atrial tachycardia (MAT) is recognized on the surface ECG by the presence of
tachycardia, at least three distinct P-waves, and at least three distinct PR intervals (Figure
132-10). Correct identification of this arrhythmia helps avoid improperly treating it as
another arrhythmia.

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Figure 132-10 Multifocal atrial tachycardia (MAT). Three or more distinct P-wave
morphologies with an irregular rhythm. (Reproduced, with permission, from Knoop KJ,
Stack LB, Storrow AB, et al. Atlas of Emergency Medicine, 3rd ed. New York, NY: McGraw-
Hill; 2009, Fig. 23-29A. Photo contributor: James V. Ritchie, MD.)

Inpatient management

Multifocal atrial tachycardia usually results from another primary problem that leads to
right heart strain or dysfunction (eg, severe COPD with exacerbation or pulmonary
embolism). By treating the underlying condition, the arrhythmia usually resolves. However,
if the tachycardia needs to be slowed based on clinical effects of the rate, β-blockers
represent the first-line treatment. A short-acting β-blocker, IV esmolol, may be considered if
concern for bronchospasm or hypotension exists. Some trials support administration of IV
magnesium to slow or convert the arrhythmia; however, this has not been well studied.
Finally verapamil is another therapeutic option, but may be limited by hypotension.
Electrical cardioversion is not effective and thus not recommended. Exacerbating factors
for MAT may include commonly used medications for COPD such as β-agonists and
theophylline.

JUNCTIONAL TACHYCARDIA

EVALUATION

Junctional tachycardia originates from the AV node or the bundle of His. The paroxysmal
form is considered a rare occurrence in the adult population, but the nonparoxysmal form
occurs most notoriously in the setting of digoxin toxicity. Particularly with digoxin toxicity,
a Wenckebach conduction block in conjunction with junctional tachycardia can manifest.
Other settings in which this arrhythmia may manifest include hypokalemia, postcardiac
surgery, chronic lung disease, myocardial ischemia, myocarditis, and rarely, underlying

sinus node dysfunction. Presentation of the arrhythmia under these circumstances allows
the clinician to differentiate it from AVnRT, AVRT, and atrial tachycardia (AT).

Inpatient management

By addressing the underlying condition, the rhythm will correct. In the setting of digoxin
toxicity, withholding the medication is the treatment of choice. Digoxin binding agents
should be considered for judicious use in the setting of ventricular arrhythmias or high-
grade AV block.

ATRIAL TACHYCARDIA
EVALUATION

An uncommon arrhythmia that falls under the category of SVT is atrial tachycardia. The
incidence of this arrhythmia in young persons is less than 1%, however this arrhythmia is
comprised of approximately 5% to 15% of patients undergoing electrophysiology studies.
The arrhythmia can be seen on 24-hour Holter monitoring, but the asymptomatic patient
should not be treated. If symptomatic, the patient may have typical symptoms
accompanied with the SVT, including palpitations, lightheadedness, dyspnea, and perhaps
syncope or presyncope.

The surface ECG can usually help differentiate AT from the more common rhythm
sinus tachycardia by the following three features. Compare the EKG’s in Figures 132-11
and 132-12 which were obtained in the same patient. The former captures an episode of
AT with a different P-wave axis and different PR interval. The second EKG, the patient is in
a sinus rhythm with a normalized P-wave axis. Review of EKG’s while not in an arrhythmia
can be helpful in identifying the SVT. The P-wave axis is usually different from the sinus P-
wave, which is upright in leads I and II. The onset and termination of atrial tachycardia is
usually very rapid, occurring over a few beats, in contrast to the 30 seconds or minutes it
takes sinus tachycardia to develop or terminate. Finally, the PR interval can be variable,
which is also known as unhooking.

Figure 132-11 Atrial tachycardia. Discernible P-waves best seen in III and aVF. Notice the
RP interval is greater than the PR interval. The tachycardia started abruptly and
spontaneously and abruptly terminated after 20 minutes.

Figure 132-12 Normal sinus rhythm of the patient after spontaneous resolution of atrial
tachycardia. Notice the distinctly different P-wave morphology between the two ECGs.

PRACTICE POINT

Atrial tachycardia features:

P-wave axis is usually different from the sinus P-wave
Onset and termination are very rapid
Occurring over a few beats (contrast to the 30 seconds or minutes it takes sinus
tachycardia to develop or terminate)
PR interval variable
Potential for developing tachycardia-induced cardiomyopathy (>70% of untreated
patients) if the incessant variety
Reversible with correction of the tachycardia

Difficulty differentiating this rhythm from a sinus tachycardia occurs when the focus
of the arrhythmia is close to the superior portion of the cristas terminalis thereby mirroring
the normal P-wave axis (positive in I, II). The importance of rhythm recognition lies in the
potential for developing a tachycardia-induced cardiomyopathy if left untreated. Some
studies have demonstrated that with an incessant form of atrial tachycardia, over 70%
patients demonstrate decreased left ventricular function. Fortunately, this complication is
reversible with correction of the tachycardia. Studies have demonstrated that patients with
early-onset atrial tachycardia (before the age of 25) frequently spontaneously develop a
normal sinus rhythm (Figure 132-12). AT could also be difficult to distinguish from AVRT
and AVnRT, but clues such as variable RP intervals make AT more likely. If in doubt, the
electrophysiologist should be consulted.

Inpatient management

In the acute setting, AV node-blocking calcium channel blockers (diltiazem, verapamil) or
β-blockers can at times terminate the arrhythmia, or simply slow the ventricular rate via
increased blockade at the AV node. Adenosine can also terminate the arrhythmia. The
alternatives that are considered efficacious are sotalol and amiodarone; however, the side
effects do need to be considered, especially if amiodarone is used for chronic
management. The vagal maneuvers usually do not work, but electrical cardioversion may
work, especially if the underlying reason for the AT is micro reentry or triggered activity.
Long-term management may include the medications discussed previously or
electrophysiologic ablation.

SINUS TACHYCARDIAS
The sinus tachycardias represent a heterogeneous group of arrhythmias comprised of
normal sinus tachycardia, inappropriate sinus tachycardia, postural orthostasis
tachycardia syndrome (POTS), and sinus node reentry tachycardia (SNRT). All have the
same ECG findings, which include a pulse rate >100 bpm, upright P-waves in limb leads I
and II (normal P-wave vector). The clinical presentation varies from the asymptomatic to
regular palpitations accompanied by syncope or presycope. Normal sinus tachycardia, as
one would expect, is a result of physiologic demand and requires the appropriate workup.

POSTURAL ORTHOSTASIS TACHYCARDIA SYNDROME

Postural orthostasis tachycardia syndrome (POTS) is usually found in a young population
between the ages of 18 and 50 with a female predominance of 5:1. The postulated

mechanisms include partial dysautonomia and the less common central β-hypersensitivity
form. POTS also has pronounced sympathetic characteristics such as tremors, anxiety,
and palpitations. The evaluation of this condition includes the head-up tilt-table (HUTT)
test documenting the patient’s symptoms and tachycardic response greater than 30 bpm
over baseline and usually greater than 120 bpm. Other diagnostic studies include 24-hour
urine sodium collection, serum norepinephrine measurement (>600 pg/dL), and
postganglionic antibody testing. The use of physical maneuvers to increase muscle tone
in the lower extremities, compression garments, volume expanders (ie, mineralocorticoids,
increased salt diet, increase fluid intake), peripheral vasoconstrictors, and centrally acting
β-blockers (ie, pindolol) are the therapeutic options, however they have limited efficacy.

INAPPROPRIATE SINUS TACHYCARDIA

Inappropriate sinus tachycardia (IST) characteristically has daytime tachycardia at rest or
with minimal exertion and normalization of the pulse during sleep. The sinus node
regulation is dysfunctional with enhanced sensitivity to sympathetic stimulus or
decreased regulation by the parasympathetic system. In contrast to sinus node reentry
tachycardia (SNRT), the onset and termination of this rhythm is gradual, and atrial
overdrive pacing has no influence on the arrhythmia. Treatment of IST requires high doses
of β-blockers or calcium channel blockers. Other treatment options include
antiarrhythmics or even catheter ablation in the event of medical failure.

SINUS NODE REENTRY TACHYCARDIA

Sinus node reentry tachycardia (SNRT) originates within or very close to the sinus node. It
usually starts and ends abruptly. Bedside interventions such as vagal maneuvers or
intravenous adenosine or verapamil can terminate this arrhythmia. Following the SVT
recognition algorithm (see Figure 132-1), this rhythm is categorized within the arrhythmias
with an RP interval greater than the PR interval.

CONSULTATION AND REFERRAL
A variety of instances of SVTs meet indications to consult general cardiology or
electrophysiology cardiology (Table 132-11).

TABLE 132-11 Consultation for Supraventricular Tachyarrhythmias

Rhythm Consult Cardiology

Consider Direct
Electrophysiology (EP)
Consult

Atrial fibrillation 1. Refractory to multiple
medications

2. Need for cardioversion
(chemical, electrical, or
both)

3. Desire to maintain sinus
rhythm

4. Lone atrial fibrillation

1. Presence of sick sinus
syndrome (SSS)—potential
ablate-pace strategy

2. Refractory to medical
management: potential for
RFA

3. Presence of pre-excitation
(WPW)

Atrial flutter 1. Refractory to multiple
medications

2. Need for cardioversion
3. Desire to maintain sinus

rhythm

Strong consideration for RFA
strategy as first-line treatment

Atrioventricular nodal
reentry tachycardia

Refractory to vagal
maneuvers and IV adenosine

Frequent and debilitating
palpitations: potential need
for RFA

Atrioventricular
tachycardia

All WPW patients 1. History of
syncope/presyncope

2. Presence of atrial
fibrillation or atrial flutter

Multifocal atrial
tachycardia

Atrial tachycardia Incessant: risk of
cardiomyopathy

Sinus tachycardia
• Sinus reentry
• Inappropriate sinus

tachycardia
• Postural orthostatic

tachycardia syndrome
(POTS)

Inability to define etiology

Junctional tachycardia Concern for digitalis toxicity

RFA, radiofrequency ablation; SSS, sick sinus syndrome; WPW, Wolff-Parkinson-White syndome.

CONCLUSION
A systematic algorithmic approach to SVTs will aid in differentiating the common from
the uncommon (see Figure 132-1). In the setting of hemodynamic instability, other
concerns fall to the wayside, and direct cardioversion should be performed without delay
(except with sinus tachycardia, where the underlying cause should be identified and
treated) (Table 132-12).

TABLE 132-12 Evidence-based Medicine: Key References for Supraventricular
Tachyarrhythmias

Reference Methodology Results Bottom Line
AFFIRM
Wyse DG, et al. N
Engl J Med.
2002;347(23):1825-
1833.

Randomized trial
(rate control vs
rhythm control for
atrial fibrillation)
• N = 4,060

No difference in
overall mortality after
5 years of follow-up
23.8% vs 21.3%
P = 0.08

Rhythm control not
better than rate
control

• Patients age >65 or
risk factors for
stroke

AF CHF
Roy D, et al. N Engl J
Med.
2008;358(25):2667-
2676.

Randomized trial
(rate control vs
rhythm control for
atrial fibrillation in
systolic CHF)
• N = 1376
• Ejection fraction

≤35%

No difference in time
to death from
cardiovascular
causes (25% vs 27%)
after 37 months

Rhythm control not
better than rate
control in systolic
CHF

Validation of Clinical
Classification
Schemes for
predicting stroke.
Gage BF, et al. JAMA.
2001;285(22):2854-
2870.

Comparison of
CHADS2 to AFI and
SPAF risk
classification
schemes

CHADS2 c statistic of
0.82 compared to
0.68 and 0.74 for AFI
and SPAF
respectively

CHADS2 performs
better at predicting
strokes than prior
classification
schemes

RE-LY: Randomized
evaluation of long-
term anticoagulation
therapy study group.
Connolly SJ, et al.
New Engl J Med.
2009;361:1139-1151.

Randomized trial in
atrial fibrillation
warfarin versu
dabigatran
• N = 18113 patients
• Dabigatran 2 doses:

110 mg twice a
day, 150 mg twice
a day

• primary outcome
• stroke or systemic

embolism
• follow-up 2 years

Coumadin event
rate= 1.69%/year
Dabigatran 110 mg =
1.53%/y
RR 0.91 P < 0.001 for noninferiority Dabigatran 150 mg = 1.11%/y RR 0.66 P < 0.001 for superiority

Higher-dose
dabigatran prevents
more strokes, but has
equal major bleeding
complications as
coumadin

CHF, congestive heart failure.

SUGGESTED READINGS
Blomström-Lundqvist C, Scheinman M, Aliot E, et al. ACC/AHA/ESC guidelines for the

management of patients with supraventricular arrhythmias: a report of the American
College of Cardiology/American Heart Association Task Force and the European Society
of Cardiology Committee for Practice Guidelines (writing committee to develop
guidelines for the management of patients with supraventricular arrhythmias). J Am
Coll Cardiol. 2003;42:1493

Fuster V, Ryden, L, Cannom M, et al. ACC/AHA/ESC 2006 guidelines for the management
of patients with atrial fibrillation: a report of the American College of

Cardiology/American Heart developed in collaboration with the European Heart Rhythm
Association and

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