1578185 - McGraw-Hill Professional ©CHAPTER 132Supravent

1578185 - McGraw-Hill Professional ©
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
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 descri be
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).
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
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
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.
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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er125.html
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
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
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.
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
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:
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
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
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 labor atory
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
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).
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
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.
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
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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1578185 - McGraw-Hill Professional ©CHAPTER 132Supravent