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C. Echocardiography
Echocardiography provides assessment of chamber volumes, LV size and function, or the presence of concomitant
valvular heart disease and should be performed in all
patients with a new diagnosis of atrial fibrillation. TEE is
the most sensitive imaging modality to identify thrombi in
the left atrium or left atrial appendage prior to any attempt
at chemical or electrical cardioversion.
» Treatment
A. Newly Diagnosed Atrial Fibrillation
1. Initial management—
a. Hemodynamically unstable patient—If the
patient is hemodynamically unstable, usually as a result of a
rapid ventricular rate or associated cardiac or noncardiac
conditions, hospitalization and immediate treatment of
atrial fibrillation are required. Intravenous beta-blockers
(esmolol, propranolol, and metoprolol) or calcium channel
blockers (diltiazem and verapamil) are usually effective at
rate control in the acute setting. Urgent electrical cardioversion is only indicated in patients with shock or severe hypotension, pulmonary edema, or ongoing MI or ischemia.
There is a potential risk of thromboembolism in patients
undergoing cardioversion who have not received anticoagulation therapy if atrial fibrillation has been present for more
than 48 hours or is of unknown duration; however, in hemo-
dynamically unstable patients the need for immediate rate
control outweighs that risk. An initial biphasic shock with at
least 200 J is administered in synchrony with the R wave. If
sinus rhythm is not restored, an additional attempt with
360 J is indicated. If this fails, cardioversion may be successful
after loading with intravenous ibutilide (1 mg over
10 minutes, repeated in 10 minutes if necessary).
b. Hemodynamically stable patient—If the patient
has no symptoms, hemodynamic instability, or evidence of
important precipitating conditions (such as silent MI or
ischemia, decompensated HF, or hemodynamically significant valvular disease), hospitalization is usually not necessary. In most of these cases, atrial fibrillation is an
unrecognized chronic or paroxysmal condition and should
be managed accordingly (see Subsequent Management,
below). For new-onset atrial fibrillation, basic blood tests
(CBC, metabolic panel, and thyroid function) and echocardiography to assess for occult valvular or myocardial disease should be performed.
In stable patients with atrial fibrillation, an initial strat-
egy of rate control and anticoagulation is often suitable. The
choice of agent is guided by the hemodynamic status of the
patient, associated conditions, and the urgency of achieving rate control. In the stable patient with atrial fibrillation,
a nondihydropyridine calcium channel blocker or betablocker (orally or intravenously) is the first-line agent for
ventricular rate control. In the setting of MI or ischemia,
beta-blockers are the preferred agent. The most frequently
used agents are either metoprolol (2.5–5 mg intravenous
bolus, repeated up to three times at intervals of 5 minutes
and then given orally at total daily doses of 25–200 mg) or,
in unstable patients, esmolol (0.5 mg/kg intravenous bolus,
followed by a titrated infusion of 0.05–0.3 mg/kg/min). If
beta-blockers are contraindicated, calcium channel blockers are rapidly effective. Diltiazem (10–20 mg bolus,
repeated after 15 minutes if necessary, followed by a maintenance infusion of 5–15 mg/hour) is the preferred calcium
blocker if hypotension is present. Otherwise, verapamil
(5–10 mg intravenously over 2–3 minutes, repeated after
30 minutes if necessary) may be used. Rate control using
digoxin is relatively slow (onset of action more than 1 hour
with peak effect at 6 hours); however, it may be useful as an
adjunct when rate control with the previously cited agents
is incomplete. Similarly, amiodarone, even when administered intravenously, has a relatively slow onset and is most
useful when cardioversion is planned in the near future.
Care should be taken in patients with hypotension or HF
because the rapid intravenous administration of amiodarone may worsen hemodynamics.
Up to two-thirds of patients experiencing acute onset
(shorter than 36 hours) of atrial fibrillation will spontaneously revert to sinus rhythm without the need for cardioversion. If atrial fibrillation has been present for more than
a week, spontaneous conversion is unlikely and cardioversion may be considered for symptomatic patients. Importantly, if the onset of atrial fibrillation was more than 48
hours prior to presentation (or unknown), a transesophageal
echocardiogram should be performed prior to cardioversion
to exclude left atrial thrombus. If thrombus is present, the
cardioversion is delayed until after a 3–6-week period of
therapeutic anticoagulation and repeated imaging. Because
atrial contractile activity may not recover for several weeks
after restoration of sinus rhythm in patients who have been
in atrial fibrillation for more than 48 hours, therapeutic
anticoagulation should be established pre-cardioversion and
continued without interruption for at least 1 month afterwards. Younger patients without HF, diabetes, hyperten-
sion, or other risk factors for stroke may not require
long-term anticoagulation.
2. Subsequent management—If immediate cardioversion
is not performed, adequate long-term rate control can usually be achieved with beta-blockers or nondihydropyridine
calcium channel blockers. Choice of the initial rate control
medication is best based on the presence of accompanying
conditions: Patients with hypertension can be given
beta-blockers or calcium blockers (see Tables 13–8, 13–10,
and 13–11). Patients with CHD or HF should receive a
beta-blocker (carvedilol, long-acting metoprolol or bisoprolol) preferentially, whereas beta-blockers should be
avoided in patients with severe COPD or asthma. Digoxin
may be used as a second agent when rate-control is inadequate with beta-blocker or calcium channel blocker alone
(target serum concentration 0.5–1.2 ng/mL). In symptomatic patients, a resting heart rate of less than 80 beats/min is
targeted. In asymptomatic patients without LV dysfunction,
a more lenient resting heart rate of 85–110 beats/min is
reasonable. Ambulatory monitoring to assess heart rate during exercise should be considered in all patients with a goal
not to exceed maximum predicted heart rate (220 – age).
a. Anticoagulation—For patients with atrial fibrillation, even when it is paroxysmal or occurs rarely, the need for
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oral anticoagulation should be evaluated and treatment
initiated for those without strong contraindication. Patients
under the age of 65 years with atrial fibrillation in the
absence of associated heart disease, hypertension, atherosclerotic vascular disease, diabetes mellitus, or history of
stroke or TIA do not require antithrombotic treatment.
Patients with transient atrial fibrillation, such as in the
setting of acute MI or pneumonia, but no prior history of
arrhythmia, are at high risk for future development of atrial
fibrillation and appropriate anticoagulation should be initiated based on risk factors. If the cause is reversible, such as
after coronary artery bypass surgery or associated with
hyperthyroidism, then long-term anticoagulation may not
be necessary.
Several risk scores based on clinical factors have been
developed to guide anticoagulant use in patients with
atrial fibrillation. The CHA2DS2- VA Sc score is considered
the most validated and includes the traditional five risk
factors that comprise the CHADS2 score (HF, hypertension, age 75 years or older, diabetes mellitus, and [2 points
for] history of stroke or TIA) with three additional factors
(age 65–74 years, female sex, and presence of vascular disease) (Table 12–2). If the CHA2DS2-VASc score is greater
than or equal to 2 in men or 3 in women, oral anticoagulation is recommended. For patients at low-moderate risk
(CHA2DS2-VASc score 1 in men, 2 in women), oral anticoagulation can be considered, taking into account risk,
benefit, and patient preferences. In patients with atrial
fibrillation and no clinical risk factors (CHA2DS2-VASc
score 0), there is no indication for anticoagulant or antithrombotic therapy. In general, unless there is an indication for antiplatelet therapy (CHD, peripheral vascular
disease), patients with atrial fibrillation should not be prescribed aspirin for stroke prevention.
Four DOACs—dabigatran, rivaroxaban, apixaban, and
edoxaban—have been shown to be at least as effective as
warfarin for stroke prevention in patients with atrial fibrillation and have been approved by the FDA for this indication (Table 12–3). These medications have not been studied
in patients with moderate or severe mitral stenosis, and
they should not be used for patients with mechanical prosthetic valves. The term “nonvalvular atrial fibrillation” is
no longer used in the American or European guidelines
since most patients with valvular heart disease (other than
mitral stenosis) have been included in trials of DOACs and
shown to be equally as effective in these patients.
Dabigatran (studied in the RE-LY trial) is superior to
warfarin at preventing stroke at the 150 mg twice daily dose,
and it is noninferior at the 110 mg twice daily dose, although
this dose is not approved for treatment of atrial fibrillation
in the United States. Both doses result in less intracranial
hemorrhage than warfarin but also in more GI bleeding than
warfarin. Neither dabigatran nor any of the DOACs should
be used in patients with mechanical prosthetic heart valves
where the medications are less effective and riskier.
Rivaroxaban is noninferior to warfarin for stroke prevention in atrial fibrillation (in the ROCKET-AF trial).
Rivaroxaban is dosed at 20 mg once daily, with a reduced
dose (15 mg/day) for patients with creatinine clearances
between 15 and 50 mL/min. It should be administered with
Table 12–2. CHA2DS2-VASc Risk Score for assessing risk
of stroke and for selecting antithrombotic therapy for
patients with atrial fibrillation.
CHA2DS2-VASc Risk Score
HF or LVEF ≤ 40% 1
Hypertension 1
Age ≥ 75 years 2
Diabetes mellitus 1
Stroke, transient ischemic attack, or
thromboembolism
Vascular disease (previous MI, peripheral artery
disease, or aortic plaque)
Age 65–74 years 1
Female sex (but not a risk factor if female sex is
the only factor)
Adjusted stroke rate according to CHA2DS2-VASc score
CHA2DS2-VASc
Score
0 1 0%
1 422 1.3%
2 1230 2.2%
3 1730 3.2%
4 1718 4.0%
5 1159 6.7%
6 679 9.8%
7 294 9.6%
8 82 6.7 %
9 14 15.2%
CHA2DS2-VASc score = 0: recommend no antithrombotic therapy
CHA2DS2-VASc score = 1 (men) or 2 (women): consider
antithrombotic therapy with oral anticoagulation
CHA2DS2-VASc score > 1 (men) or > 2 (women): recommend
antithrombotic therapy with oral anticoagulation
CHA2DS2-VASc, Cardiac failure, Hypertension, Age ≥ 75 years
(doubled), Diabetes, Stroke (doubled), Vascular disease, Age 65–74,
and Sex category (female).
Data from Camm AJ et al. 2012 focused update of the ESC
Guidelines for the management of atrial fibrillation: an update of
the 2010 ESC Guidelines for the management of atrial fibrillation.
Patients
(n = 7329)
2
1
1
Adjusted
stroke rate
(%/year)
food, since that results in a 40% higher drug absorption. As
with dabigatran, there is substantially less risk of intracranial hemorrhage with rivaroxaban than warfarin.
Apixaban is more effective than warfarin at stroke prevention while having a substantially lower risk of major
bleeding (in the ARISTOTLE trial) and a lower risk of allcause mortality. The apixaban dosage is 5 mg twice daily or
2.5 mg twice daily for patients with two of three high-risk
criteria (age 80 years or older, body weight 60 kg or less,
and serum creatinine of 1.5 mg/dL or more). Apixaban is
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Table 12–3. DOACs for stroke prevention in patients with atrial fibrillation. (Listed in alphabetical order.)
Apixaban Dabigatran Edoxaban Rivaroxaban
Class Factor Xa inhibitor Antithrombin Factor Xa inhibitor Factor Xa inhibitor
Bleeding risk compared
to warfarin
Dosage 5 mg twice daily 150 mg twice daily 60 mg once daily 20 mg once daily
Dosage adjustments 2.5 mg twice daily for
1
Creatinine clearance calculated by Cockcroft-Gault equation.
Data from Nishimura RA et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):e521–643.
Substantially lower risk of
major bleeding
Less intracranial bleeding
patients with at least two
of three risk factors:
1. Age ≥ 80 years
2. Body weight ≤ 60 kg
3. Serum creatinine
≥ 1.5 mg/dL
Less intracranial bleeding
Higher incidence of GI
bleeding
75 mg twice daily for
creatinine clearance1
15–30 mL/min
Lower risk of major
bleeding
Less intracranial bleeding
30 mg once daily for
creatinine clearance1
≤ 50 mL/min
FDA recommends not to
use if creatinine clearance1 > 95 mL/min
Less intracranial bleeding
Higher incidence of GI
bleeding
(give with food)
15 mg once daily for
creatinine clearance1
< 50 mL/min
associated with less intracranial hemorrhage and is well
tolerated. Apixaban has been studied in a small trial of
patients receiving hemodialysis, with pharmacokinetic
studies suggesting a dose of 2.5 mg twice daily in these
patients results in equivalent serum concentrations as 5 mg
twice daily in patients with normal kidney function.
Edoxaban, 60 mg once a day, is noninferior to warfarin
for stroke prevention with lower rates of major bleeding
and lower rates of hemorrhagic stroke (studied in the
ENGAGE-AF trial). Edoxaban carries a boxed warning in
FDA labelleling that it should not be used in patients whose
creatinine clearance is more than 95 mL/min because it is
less effective in this population. The dose is decreased to
30 mg/day for patients whose creatinine clearance is less
than or equal to 50 mL/min.
These four DOACs have important advantages over warfarin, and therefore, they are recommended preferentially
over vitamin K antagonists (VKAs). In practice, these medi-
cations are often underdosed. They should be used at the
doses shown to be effective in the clinical trials as shown in
Table 12–3. Even though labeled for “nonvalvular” atrial
fibrillation, the DOACs are safe and effective for patients
with moderate or severe valvular abnormalities, apart from
moderate or severe mitral stenosis. In part because of lower
rates of intracerebral hemorrhage, DOACs have particular
advantage over warfarin in older adults and frail patients,
including patients with history of falls. For patients who fall,
shared-decision making weighing risks and benefits should
be incorporated. However, oral anticoagulation should
generally be continued.
Warfarin remains first-line therapy in patients who
have mechanical prosthetic valves, moderate or severe
mitral stenosis, and those who cannot afford DOACs.
Patients who have been stable while receiving warfarin for
a long time, with a high time in target INR range, and who
are at lower risk for intracranial hemorrhage will have relatively less benefit with a switch to a DOAC. One way to
reduce bleeding for patients taking oral anticoagulants is to
avoid concurrent aspirin, unless there is a clear indication,
like recent MI or coronary stent. Even then, use of oral
anticoagulant plus clopidogrel without aspirin, or with
only a brief period of “triple” therapy and then discontinuation of aspirin, may be a reasonable approach.
There are some important practical issues with using
the DOACs. It is important to monitor blood counts and
kidney function at baseline and at least twice a year, or more
often for those with impaired kidney function. Each of the
DOACs interacts with other medications affecting the
P-glycoprotein pathway, such as oral ketoconazole, verapamil, dronederone, and phenytoin. To transition patients
from warfarin to a DOAC, wait until the INR decreases to
about 2.0. Each of the medications has a half-life of about
10–12 hours for patients with normal kidney function. For
elective procedures, stop the medications two to three halflives (usually 24–48 hours) before procedures with low to
moderate bleeding risk (ie, colonoscopy, dental extraction,
cardiac catheterization), and five half-lives before major
surgery. Discontinuation times should be extended in patients
with impaired renal function, particularly with dabigatran.
For patients discontinuing DOAC peri-procedurally, there
is no need for bridging anticoagulation. While there are no
practical tests to immediately measure the anticoagulant
effect of the medications, a normal aPTT suggests little
effect with dabigatran, and a normal prothrombin suggests
little effect with rivaroxaban. Routine measurement of
DOAC plasma concentrations is not recommended due to
lack of established therapeutic ranges.
Approximately 2–4% of patients on oral anticoagulation have major bleeding which may require intervention.
For bleeding, standard measures (ie, diagnosing and controlling the source, stopping antithrombotic agents, and
replacing blood products) should be taken. If the DOAC
was taken in the prior 6–8 hours, activated oral charcoal
may be used to reduce absorption. If the patient is taking
aspirin, consider platelet transfusion. Due to the short halflife of the DOACs (10–12 hours with normal kidney
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function), supportive measures (local control, packed
RBCs, platelets) may suffice until the medication has
cleared. Antidotes should be considered for life-threatening
bleeding or for patients with need for immediate surgery.
A patient with severe bleeding while taking dabigatran may
be treated with the reversal agent idarucizumab (given as
5 g IV infusion over 5 minutes), a humanized monoclonal
antibody that binds the medication resulting in rapid
reversal of its anticoagulation effect. Andexanet alfa (given
as 400 mg bolus at a rate of 30 mg/min followed by 4 mg/
min for up to 120 minutes), a factor Xa decoy, is FDAapproved for reversal of the factor Xa inhibitors rivaroxaban and apixaban. For life-threatening bleeding with
warfarin or other VKAs, four-factor prothrombin com-
plex concentrate in addition to intravenous vitamin K may
partially reverse the anticoagulant effect and is preferred
over fresh frozen plasma.
In patients who are unsuitable for long-term anticoagulation due to excessive bleeding risk, left atrial appendage
occluders (including the Watchman and Amulet devices)
have been shown to protect against stroke, although they
may not be as effective as warfarin in preventing ischemic
stroke. Occlusion of the left atrial appendage during cardiac surgery provides further protection against ischemic
stroke over and above ongoing oral anticoagulant use.
b. Rate control or rhythm control—After assessing
stroke risk and initiating anticoagulation where appropriate, two main treatment strategies for long-term management of atrial fibrillation exist: rate control or rhythm
control, although they are not mutually exclusive. Rate
control should be considered background treatment in nearly
all patients with atrial fibrillation, regardless of whether
rhythm restoration is eventually pursued, and may be considered the primary treatment in patients with minimal to no
symptoms related to long-standing atrial fibrillation. In
patients with recent-onset atrial fibrillation (less than 1
year), the EAST-AFNET 4 trial found that rhythm control
with antiarrhythmic medication or catheter ablation is
associated with a lower risk of death from cardiovascular
causes, stroke, or hospitalization for HF.
The decision to pursue rhythm control is often individualized, based on symptoms, the type of atrial fibrillation (paroxysmal or persistent), comorbidities (such as
HF), as well as general health status. As first treatment,
elective cardioversion (200 J or more, biphasic energy) is
recommended in patients in whom atrial fibrillation is
thought to be of recent onset or when there is an identifiable precipitating factor. Similarly, cardioversion is appropriate in patients who remain symptomatic from the
rhythm despite efforts to achieve rate control. In patients
with atrial fibrillation duration of greater than 48 hours (or
unknown), a minimum of 3 weeks of anticoagulation or
exclusion of left atrial thrombus by TEE pre-cardioversion
is required. Anticoagulation should be continued for at
least 4 weeks following cardioversion to prevent thromboembolism. In patients with prior left atrial appendage
occlusion, data on peri-cardioversion stroke risk and anticoagulation strategies are lacking. However, TEE is recommended to exclude device-related thrombus or peri-device
leak which may prompt anticoagulant initiation.
In cases in which elective cardioversion is required, it
may be accomplished pharmacologically or electrically.
Pharmacologic cardioversion with intravenous ibutilide
(1 mg over 10 minutes, repeated in 10 minutes if necessary)
or procainamide (15 mg/kg over 30 minutes) may be used
in a setting in which the patient can undergo continuous
ECG monitoring for at least 4–6 hours following administration. Pretreatment with intravenous magnesium (1–2 g)
may prevent rare episodes of torsades de pointes associated
with ibutilide administration. The incidence of torsades de
pointes with ibutilide is higher in patients with reduced
cardiac function and therefore its use should be avoided in
patients with LV EF 40% or less. In patients in whom a decision has been made to continue antiarrhythmic therapy to
maintain sinus rhythm (see next paragraph), cardioversion
can be attempted with an agent that is being considered for
long-term use. For instance, after therapeutic anticoagulation has been established, amiodarone can be initiated on
an outpatient basis (400 mg twice daily for 2 weeks, followed by 200 mg twice daily for at least 2–4 weeks and then
a maintenance dose of 200 mg daily). Because amiodarone
increases the prothrombin time in patients taking warfarin
and increases digoxin levels, careful monitoring of anticoagulation and medication levels is required.
Other antiarrhythmic medications that can be used for
long-term maintenance therapy include propafenone, flecainide, dronedarone, dofetilide, and sotalol. Dofetilide
(125–500 mcg twice daily orally) must be initiated in hospital due to the potential risk of torsades de pointes and the
downward dose adjustment that is required for patients
with significant QT interval prolongation. Propafenone
(150–300 mg orally every 8 hours) and flecainide (50–150
mg orally twice daily) should be avoided in patients with
structural heart disease (CHD, systolic dysfunction, or
significant LVH) and should be used in conjunction with
an AV nodal blocking medication, especially if there is a
history of atrial flutter. Sotalol (80–160 mg orally twice
daily) should be initiated in the hospital in patients with
structural heart disease due to a risk of torsades de pointes;
it is not very effective for converting atrial fibrillation but
can be used to maintain sinus rhythm following cardioversion. Dronedarone should not be used in patients with
recent decompensated HF or when atrial fibrillation has
become persistent.
In patients treated long-term with an antiarrhythmic
agent, sinus rhythm will persist in 30–50%. Given this high
rate of arrhythmia recurrence, the decision to maintain
long-term anticoagulation should be based on risk factors
(CHA2DS2-VASc score, Table 12–2) and not on the perceived presence or absence of atrial fibrillation, since future
episodes may be asymptomatic.
B. Recurrent and Refractory Atrial Fibrillation
1. Recurrent paroxysmal atrial fibrillation—For select
patients with symptomatic but rare (a few times a year)
episodes of atrial fibrillation, an effective treatment strategy is on-demand pharmacologic cardioversion, termed
pill-in-the-pocket treatment. Patients without coronary
or structural heart disease may be given flecainide (200–
300 mg) or propafenone (450–600 mg) in addition to a
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beta-blocker or nondihydropyridine calcium channel
blocker as a single dose at the onset of symptoms. It is recommended that the first such treatment take place in a
monitored setting (eg, the emergency department or
hospital) to evaluate safety and effectiveness. For more
frequent, symptomatic arrhythmic episodes, daily antiarrhythmic agents are first-line therapy; however, they are
not often successful in preventing all paroxysmal atrial
fibrillation episodes and long-term tolerability is poor.
2. Refractory atrial fibrillation—Atrial fibrillation should
be considered refractory if it causes persistent symptoms or
limits activity despite attempts at rate or rhythm control. If
antiarrhythmic or rate control medications fail to improve
symptoms, catheter ablation around the pulmonary veins
to isolate the triggers that initiate and maintain atrial fibrillation may be considered. It is a reasonable therapy for
individuals with symptomatic paroxysmal or persistent
atrial fibrillation that is refractory to pharmacologic therapy and for select patients (younger than 65 years or with
concurrent HF) as first-line therapy. The primary benefit of
catheter ablation is an improvement in quality of life. In the
CABANA trial, there was no difference in the primary
endpoint of death, disabling stroke, serious bleeding, or
cardiac arrest in patients randomized to catheter ablation
versus medical therapy as first treatment for symptomatic
atrial fibrillation. Ablation is successful about 50–70% of
the time but repeat ablation may be required in up to 20%
of patients. The procedure is routinely performed in the
electrophysiology laboratory using a catheter-based
approach and adverse event rates are low when performed
by experienced operators. Surgical ablation can also be
performed via a subxiphoid approach, thorascopically via
thoracotomy, or via median sternotomy in the operating
room as a stand-alone or adjunct procedure. Finally, in
symptomatic patients with poor rate control and deemed
inappropriate for pulmonary vein isolation, radiofre-
quency ablation of the AV node and permanent pacing
ensure rate control and may facilitate a more physiologic
rate response to activity, but this is usually performed only
after other therapies have failed.
» When to Refer
• Symptomatic atrial fibrillation with or without adequate rate control.
• Asymptomatic atrial fibrillation with poor rate control
despite AV nodal blockers.
• Patients at risk for stroke who have not tolerated oral
anticoagulants.
Joglar J et al. 2023 ACC/AHA/ACCP/HRS guideline for the
diagnosis and management of atrial fibrillation. Circulation.
2024;149:e1. [PMID: 38033089]
Parkash R et al. Randomized ablation-based rhythm-control
versus rate-control trial in patients with heart failure and
atrial fibrillation: results from the RAFT-AF trial. Circulation.
2022;145:1693. [PMID: 35313733]
Whitlock RP et al. Left atrial appendage occlusion during car-
diac surgery to prevent stroke. N Engl J Med. 2021;384:2081.
[PMID: 33999547]
ATRIAL FLUTTER
ESSENTIALS OF DIAGNOSIS
»
Rapid, regular tachycardia presenting classically
with 2 to 1 block in the AV node and ventricular
heart rate of 150 beats/min.
»
ECG shows “sawtooth” pattern of atrial activity
(rate 300 beats/min).
»
Stroke risk should be considered equivalent to
that with atrial fibrillation.
»
Catheter ablation is highly successful and is considered the definitive treatment for typical atrial
flutter.
» General Considerations
Atrial flutter is less common than fibrillation. It may occur
in patients with structurally normal hearts but is more
commonly seen in patients with COPD, valvular or structural heart disease, ASD, or surgically repaired congenital
heart disease.
» Clinical Findings
Patients typically present with reports of palpitations,
fatigue, or mild dizziness. In situations where the arrhythmia is unrecognized for a prolonged period of time, symptoms and signs of HF (dyspnea, exertional intolerance,
edema) due to tachycardia-induced cardiomyopathy may
develop. The ECG typically demonstrates a “sawtoot h” pattern
of atrial activity in the inferior leads (II, III, and AVF). The
reentrant circuit generates atrial rates of 250–350 beats/
min, usually with transmission of every second, third, or
fourth impulse through the AV node to the ventricles.
» Treatment
Ventricular rate control is accomplished using the same
agents used in atrial fibrillation, but it is generally more
difficult. Conversion of atrial flutter to sinus rhythm with
class I antiarrhythmic agents is also difficult to achieve, and
administration of these medications has been associated
with slowing of the atrial flutter rate to the point at which
1:1 AV conduction can occur at rates in excess of 200 beats/
min, with subsequent hemodynamic collapse. The intravenous class III antiarrhythmic agent ibutilide has been significantly more successful in converting atrial flutter (see
Table 12–1). About 50–70% of patients return to sinus
rhythm within 60–90 minutes following the infusion of
this agent. Electrical cardioversion is also very effective for
atrial flutter, with approximately 90% of patients converting following synchronized shocks of 100–200 J.
Although the organization of atrial contractile function
in this arrhythmia may provide some protection against
thrombus formation, the risk of thromboembolism should be
considered equivalent to that with atrial fibrillation due to
the common coexistence of these arrhythmias. As with
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atrial fibrillation, anticoagulation should be established for
at least 3 weeks or thrombus excluded with TEE precardioversion for atrial flutter of greater than 48 hours or of
unknown duration. Anticoagulation should be continued
for at least 4 weeks after electrical or chemical cardioversion and chronically in patients with risk factors for
thromboembolism.
Catheter ablation is the treatment of choice for long-term
management of atrial flutter owing to the high success rate
and safety of the procedure. The anatomy of the typical
circuit is well defined and catheter ablation within the right
atrium results in immediate and permanent elimination of
atrial flutter in more than 90% of patients. Due to the frequent coexistence of atrial flutter with atrial fibrillation,
however, some patients may require catheter ablation of
both arrhythmias. If pharmacologic therapy is chosen,
class III antiarrhythmics (amiodarone or dofetilide) are
generally preferred (see Table 12–1).
» When to Refer
All patients with atrial flutter should be referred to a cardiologist or cardiac electrophysiologist for consideration of
definitive treatment with catheter ablation.
ATRIAL TACHYCARDIA
ESSENTIALS OF DIAGNOSIS
»
Characterized by bursts of rapid, regular
tachycardia.
»
Multifocal atrial tachycardia commonly seen with
severe COPD and presents with three or more
distinct P wave morphologies on ECG, often confused for atrial fibrillation.
»
Treatment of the underlying lung disease is most
effective therapy.
» Clinical Findings
Focal atrial tachycardias are usually intermittent and selflimiting although incessant forms do exist and may present
with signs and symptoms of HF due to tachycardiainduced cardiomyopathy. Most patients report palpitations
with an abrupt onset, similar to other forms of PSVT.
Patients with underlying cardiac pathology (eg, CHD) can
present with dyspnea or angina. Close inspection of the
P wave on 12-lead ECG suggests a focus away from the
sinus node, although certain locations (eg, high right atrial
crista terminalis) may mimic sinus tachycardia. In this situation, the abrupt onset and offset of the arrhythmia are
helpful in distinguishing atrial from sinus tachycardia,
although electrophysiologic study is sometimes necessary.
» Treatment
Initial management of atrial tachycardia is similar to other
types of PSVT; however, vagal maneuvers and intravenous
adenosine are generally less effective. Intravenous betablockers or calcium channel blockers can be given in the
hemodynamically stable patient with a transition to oral
formulations for long-term management. Antiarrhythmic
medications or catheter ablation should be considered in
patients who continue to have symptomatic episodes.
Long-term anticoagulation is not indicated in the absence
of coexistent atrial fibrillation or atrial flutter.
For patients with multifocal atrial tachycardia, treatment of the underlying condition (eg, COPD) is paramount; verapamil, 240–480 mg orally daily in divided
doses, may be effective in some patients.
» When to Refer
All patients with atrial tachycardia in whom initial medical
management fails should be referred to a cardiologist or
cardiac electrophysiologist.
VENTRICULAR PREMATURE BEATS
(Ventricular Extrasystoles)
» General Considerations
Atrial tachycardia is an uncommon form of SVT characterized by paroxysms or bursts of rapid, regular arrhythmia
due to focal atrial impulses originating outside of the normal sinus node. Common sites include the tricuspid annulus, the crista terminalis of the right atrium and the
coronary sinus. Multifocal atrial tachycardia is a particu-
lar subtype seen in patients with severe COPD and characterized by varying P wave morphology (by definition, three
or more foci) and markedly irregular PP intervals. The rate
is usually between 100 beats/min and 140 beats/min, and it
is often confused for atrial fibrillation. Solitary atrial pre-
mature beats are benign and generally not associated with
underlying cardiac disease. They occur when an ectopic
focus in the atria fires before the next sinus node impulse.
The contour of the P wave usually differs from the patient’s
normal complex, unless the ectopic focus is near the sinus
node. Acceleration of the heart rate by any means usually
abolishes most premature beats.
ESSENTIALS OF DIAGNOSIS
»
Common but rarely symptomatic.
»
Ambulatory ECG monitoring to quantify daily burden of PVCs.
»
Asymptomatic patients with > 10% PVC burden
should have periodic echocardiogram to exclude
development of LV dysfunction.
» General Considerations
Ventricular premature beats, or PVCs, are isolated beats
typically originating from the outflow tract or His-Purkinje
regions of ventricular tissue. In most patients, the presence
of PVCs is a benign finding; however, they rarely may trigger ventricular tachycardia or ventricular fibrillation, especially in patients with underlying heart disease.
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» Clinical Findings
Patients may be asymptomatic or experience palpitations,
dizziness, or vague chest pain. Some patients feel the
irregular beat; however, symptoms can often be secondary
to post-PVC augmentation of contractility or a post-PVC
compensatory pause. Increase in the sinus rate with exercise generally abolishes premature beats in normal hearts.
PVCs are characterized by wide QRS complexes that differ
in morphology from the patient’s normal beats. They are
usually not preceded by a P wave, although retrograde
ventriculoatrial conduction may occur. Bigeminy and
trigeminy are arrhythmias in which every second or third
beat is premature. Ambulatory ECG monitoring may
reveal more frequent and complex PVCs than occur in a
single routine ECG. An increased frequency of PVCs during
exercise is associated with a higher risk of cardiovascular
mortality and should be investigated further.
» Treatment
If no associated cardiac disease is present and if the ectopic
beats are asymptomatic, no therapy is indicated. Mild
symptoms or anxiety from palpitations may be allayed with
reassurance to the patient of the benign nature of this
arrhythmia. If PVCs are frequent (bigeminal or trigeminal
pattern) or multifocal, electrolyte abnormalities (ie, hypoor hyperkalemia and hypomagnesemia) and occult cardiac
disease (ie, ischemic heart disease or LV dysfunction)
should be excluded. In addition, an echocardiogram should
be performed in patients in whom a burden of PVCs of
greater than 10,000 per day has been documented by ambulatory ECG monitoring. Pharmacologic treatment is indicated only for patients who are symptomatic or who
develop cardiomyopathy thought to be due to a high burden
of PVCs (generally greater than 10% of daily heart beats).
Beta-blockers or nondihydropyridine calcium channel
blockers are appropriate as first-line therapy. The class I and
III antiarrhythmic agents (see Table 12–1) may be effective
in reducing PVCs but are often poorly tolerated and can be
proarrhythmic in up to 5% of patients. Catheter ablation is
a well-established therapy for symptomatic individuals who
do not respond to medication or for those patients whose
burden of ectopic beats has resulted in a cardiomyopathy.
» When to Refer
Patients with symptomatic PVCs who do not respond to
initial medical management or asymptomatic patients with
daily PVC burden greater than 10% on ambulatory ECG
monitoring should be referred to a cardiologist or cardiac
electrophysiologist.
VENTRICULAR TACHYCARDIA
ESSENTIALS OF DIAGNOSIS
»
Fast, wide QRS complex on ECG.
»
Associated with ischemic heart disease, particularly in older patients.
»
In the absence of reversible cause, implantable
cardioverter defibrillator (ICD) is recommended if
meaningful life expectancy is > 1 year.
» General Considerations
Ventricular tachycardia is defined as three or more consecutive ventricular premature beats. It is classified as
either nonsustained (lasting less than 30 seconds and terminating spontaneously) or sustained with a heart rate
greater than 100 beats/min. In individuals without heart
disease, nonsustained ventricular tachycardia is generally
associated with a benign prognosis. In patients with structural heart disease, nonsustained ventricular tachycardia is
associated with an increased risk of subsequent symptomatic ventricular tachycardia and sudden death, especially
when seen more than 48 hours after MI.
Ventricular tachycardia is a frequent complication of
acute MI and dilated cardiomyopathy but may occur in
chronic coronary disease, HCM, myocarditis, and in most
other forms of myocardial disease. It can also be a consequence of atypical forms of cardiomyopathies, such as
arrhythmogenic RV cardiomyopathy. However, idiopathic
ventricular tachycardia can also occur in patients with
structurally normal hearts. Accelerated idioventricular
rhythm is a regular wide-complex rhythm with a rate of
60–120 beats/min, usually with a gradual onset. It occurs
commonly in acute infarction and following reperfusion
with thrombolytic medications. Treatment is not indicated
unless there is hemodynamic compromise or more serious
arrhythmias. Torsades de pointes, a form of ventricular
tachycardia in which the QRS morphology twists around
the baseline, may occur in the setting of severe hypokalemia, hypomagnesemia, or in the setting of a prolonged QT
interval (inherited or medication-induced).
» Clinical Findings
A. Symptoms and Signs
Patients commonly experience palpitations, dyspnea, or
lightheadedness, but on rare occasion may be asymptomatic. Syncope or cardiac arrest can be presenting symptoms
in patients with underlying cardiac disease or other severe
comorbidities. Episodes may be triggered by exercise or
emotional stress.
B. Diagnostic Studies
Comprehensive blood laboratory work should be performed because ventricular tachycardia can occur in the
setting of hypokalemia and hypomagnesemia. Cardiac
markers may be elevated when ventricular tachycardia
presents in the setting of acute MI or as a consequence of
underlying CAD and demand ischemia. In patients with
sustained, hemodynamically tolerated ventricular tachycardia, a 12-lead ECG during tachycardia should be
obtained. Cardiac evaluation with echocardiography or
cardiac MRI, ambulatory ECG monitoring, and exercise
testing may be warranted depending on the clinical situation. Survivors of cardiac arrest or life-threatening
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ventricular arrhythmia should be evaluated for ischemic
heart disease (CT or invasive coronary angiography) and
undergo revascularization when appropriate.
There is generally no role for invasive electrophysiologic study in patients with sustained ventricular tachycardia who otherwise meet criteria for ICD. In patients with
structural heart disease and syncope of unknown cause, or
in situations in which the mechanism of wide-complex
tachycardia is uncertain, electrophysiologic study may provide important information.
C. Differentiation of Aberrantly Conducted
Supraventricular Beats from Ventricular Beats
The distinction on 12-lead ECG of ventricular tachycardia
from SVT with aberrant conduction may be difficult in
patients with a wide-complex tachycardia; it is important
because of the differing prognostic and therapeutic implications of each type. Findings favoring a ventricular origin
include: (1) AV dissociation; (2) a QRS duration exceeding
0.14 second; (3) sinus capture or fusion beats; (4) left axis
deviation with right bundle branch block morphology; (5)
monophasic (R) or biphasic (qR, QR, or RS) complexes in
V1; and (6) a qR or QS complex in V6. Supraventricular
origin is favored by: (1) a typical right or left bundle
branch block morphology; (2) QRS duration less than 0.14
second; and (3) the presence of preexcitation syndrome by
history or on prior ECG. Patients with a wide-complex
tachycardia, especially those with known cardiac disease,
should be presumed to have ventricular tachycardia if the
diagnosis is unclear.
» Treatment
A. Initial Management
The treatment of acute ventricular tachycardia is determined by the degree of hemodynamic compromise and the
duration of the arrhythmia. In patients with structurally
normal hearts, the prognosis is generally benign and syncope is uncommon. The etiology is often triggered activity
from the RV or LV outflow tract, and immediate treatment
with a short-acting intravenous beta-blocker or verapamil
may terminate the episode.
In the presence of known or suspected structural heart
disease, assessment of hemodynamic stability determines
the need for urgent direct current cardioversion. When
ventricular tachycardia causes hypotension, HF, or myocardial ischemia, immediate synchronized direct current
cardioversion with 100–200 J should be performed. If
ventricular tachycardia recurs, intravenous amiodarone
(150-mg bolus followed by 1 mg/min infusion for 6 hours
and then 0.5 mg/min for 18 hours) should be administered
to achieve a stable rhythm with further attempts at cardioversion as necessary. Significant hypotension can occur
with rapid infusions of amiodarone.
In patients with sustained ventricular tachycardia who
are hemodynamically stable, medical treatment with intravenous amiodarone, lidocaine, or procainamide can be
used; however, direct current cardioversion should be
performed if the ventricular tachycardia fails to terminate
or symptoms worsen. Empiric magnesium replacement
(1–2 g intravenously) may help, especially for polymorphic
ventricular tachycardia. If polymorphic ventricular tachycardia recurs, increasing the heart rate with isoproterenol
infusion (up to 20 mcg/min) or atrial pacing with a temporary pacemaker (at 90–120 beats/min) will effectively
shorten the QT interval to prevent further episodes. In
patients with polymorphic ventricular tachycardia in the
setting of a normal QT interval, myocardial ischemia
should be considered with prompt evaluation and coronary
revascularization performed as indicated.
B. Long-Term Management
Patients with symptomatic or sustained ventricular tachycardia in the absence of a reversible precipitating cause
(acute MI or ischemia, electrolyte imbalance, medication
toxicity, etc) are at high risk for recurrence. In patients with
structurally normal hearts and ventricular tachycardia with
typical outflow tract (left bundle branch block with inferior
axis) or left posterior fascicle (right bundle branch block
with superior axis) appearance on ECG, suppressive treatment with beta-blocker or a nondihydropyridine calcium
channel blocker may be tried. Catheter ablation has a high
success rate in these patients who fail initial medical treatment. In patients with significant LV dysfunction, subsequent sudden death is common and ICD implantation is
recommended if meaningful survival is expected to be
longer than 1 year. Beta-blockers are the mainstay for
medical treatment of ventricular tachycardia in patients
with structural heart disease. Antiarrhythmic medications
(eg, amiodarone or sotalol) have not been shown to lower
mortality in these patients but may decrease subsequent
episodes and reduce the number of ICD shocks. Catheter
ablation is an important treatment option for those patients
with recurrent tachycardia who do not respond to or are
intolerant of medical therapy. Owing to the potential side
effects from long-term antiarrhythmic use, catheter ablation may be considered as a first-line treatment especially
for patients with ischemic cardiomyopathy.
» When to Refer
Any patient with sustained ventricular tachycardia or syncope of unknown cause in the presence of underlying
structural cardiac disease.
Arenal Á et al. 2022 Substrate ablation vs antiarrhythmic drug
therapy for symptomatic ventricular tachycardia. J Am Coll
Cardiol. 2022;79:1441. [PMID: 35422240]
VENTRICULAR FIBRILLATION &
SUDDEN DEATH
ESSENTIALS OF DIAGNOSIS
»
Most patients with SCD have underlying CHD.
»
In the absence of reversible cause, ICD is
recommended.
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» General Considerations
SCD is defined as unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after
onset of symptoms. The causative rhythm in most cases is
ventricular fibrillation. Sudden cardiac arrest is a term
reserved for the successful resuscitation of patients with
ventricular fibrillation, either spontaneously or via intervention (defibrillation).
» Clinical Findings
Approximately 70% of cases of SCD are attributable to
underlying CHD; in up to 40% of patients, SCD may be
the initial manifestation of CHD. In patients younger than
35, most cases of SCD are caused by inherited heart disease (long QT syndrome, catecholaminergic polymorphic
ventricular tachycardia, Brugada syndrome, HCM,
arrhythmogenic RV cardiomyopathy, dilated cardiomyopathy). Over the age of 35, CHD is the most common
cause of SCD, although inherited causes are common up
until the age of 50. Noninherited forms of heart disease
can also lead to SCD, including valvular heart disease
(aortic stenosis, pulmonic stenosis), congenital heart disease, and myocarditis. Prompt evaluation to exclude
reversible causes of sudden cardiac arrest should begin
immediately following resuscitation. Laboratory testing
should be performed to exclude severe electrolyte abnormalities (particularly hypokalemia and hypomagnesemia)
and acidosis and to evaluate cardiac biomarkers. Caution
should be taken in attributing cardiac arrest solely to an
electrolyte disturbance, however, because laboratory
abnormalities may be secondary to resuscitation and not
causative of the event. A 12-lead ECG should be performed to evaluate for ongoing ischemia or conduction
system disease. Ventricular function should be evaluated
with echocardiography. Evaluation for ischemic heart disease (CT or coronary angiography) should be performed
to exclude coronary disease as the underlying cause, since
revascularization may prevent recurrence. In the absence
of coronary disease, contrast-enhanced cardiac MRI may
be used to evaluate for the presence of myocardial scar,
which is a strong predictor of recurrent ventricular
tachycardia/ventricular fibrillation in patients with
nonischemic cardiomyopathy.
» Treatment
Unless ventricular fibrillation occurs shortly after MI, is
associated with ischemia, or is seen with a correctable process (such as an electrolyte abnormality or medication
toxicity), surviving patients require intervention since
recurrences are frequent. Survivors of cardiac arrest have
improved long-term outcomes if a targeted temperature
management protocol is rapidly initiated and continued
for 24–36 hours after cardiac arrest.
Patients who survive sudden cardiac arrest have a high
incidence of recurrence, so an ICD is generally indicated.
Sudden cardiac arrest in the setting of acute ischemia or
infarct should be managed with prompt coronary
revascularization. However, implantation of a prophylactic
ICD in patients immediately after MI is associated with a
trend toward worse outcomes. These patients may be managed with a wearable cardioverter defibrillator until
recovery of ventricular function can be assessed by echocardiogram at a later date (6–12 weeks following MI or
coronary intervention). In patients in whom ventricular
function remains low (EF less than or equal to 35%), a
permanent subcutaneous ICD (when pacing is not
required) or transvenous ICD should be implanted.
» When to Refer
All survivors of sudden cardiac arrest should be referred to
a cardiologist or cardiac electrophysiologist.
INHERITED ARRHYTHMIA SYNDROMES
ESSENTIALS OF DIAGNOSIS
»
Includes long QT syndrome, Brugada syndrome,
arrhythmogenic RV cardiomyopathy, and catecholaminergic polymorphic ventricular tachycardia.
»
Genetic testing for patients with suspected congenital long QT syndrome based on family history,
ECG or exercise testing, or severely prolonged QT
interval (greater than 500 msec) on serial ECGs.
»
Patients with long QT syndrome or catecholaminergic polymorphic ventricular tachycardia should
be treated long term with an oral beta-blocker
(nadolol or propranolol).
»
ICD is indicated for patients with ventricular
arrhythmia or syncope despite medical treatment.
» General Considerations
Inherited arrhythmia syndromes may result in life-threatening ventricular arrhythmias due to gene mutations in
cardiac channels resulting in abnormal electrolyte regulation across the cardiac cell membrane. Congenital long
QT syndrome is an uncommon disease (1 in 2500 live
births) that is characterized by a long QT interval (usually
greater than 470 msec) and ventricular arrhythmia, typically polymorphic ventricular tachycardia. Acquired long
QT syndrome is usually secondary to use of antiarrhythmic agents (sotalol, dofetilide), methadone, antidepressant
medications, or certain antibiotics; electrolyte abnormalities; myocardial ischemia; or significant bradycardia.
Brugada syndrome accounts for up to 20% of SCD in the
absence of structural heart disease and is most often due to
a defect in a sodium channel gene. Arrhythmogenic RV
cardiomyopathy is an inherited cardiomyopathy that predominantly affects the RV and is characterized by areas of
myocardial replacement with fibrosis and adipose tissue
that frequently causes ventricular arrhythmia. Catechol-
aminergic polymorphic ventricular tachycardia is a rare
but important cause of SCD associated with exercise.
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» Clinical Findings
Patients with an inherited arrhythmia syndrome have a
variable clinical presentation; they may be asymptomatic
or have palpitations, sustained tachyarrhythmia, syncope,
or sudden cardiac arrest. In young patients, syncopal episodes may be misdiagnosed as a primary seizure disorder.
Personal and family history should be thoroughly reviewed
in all patients. A 12-lead ECG should be performed with
careful attention to any abnormality in the ST segment, T
wave, and QT interval. A corrected QT interval longer than
500 msec on serial ECGs in the absence of a secondary
cause (medication or electrolyte abnormality) identifies a
high-risk subset of patients with long QT syndrome.
Ambulatory ECG monitoring may be used to evaluate for
ventricular arrhythmias as well as dynamic changes to the
QT interval or T wave. Exercise ECG testing may be performed in patients with suspected long QT syndrome to
assess for lack of appropriate QT interval shortening with
higher heart rates. In cases where the cause of sudden cardiac arrest is suspected to be heritable, genetic testing
under the guidance of a multidisciplinary genetics team is
recommended to both determine the diagnosis and to
facilitate the identification of first-degree family members
at risk for developing the same disease.
» Treatment
Management of polymorphic ventricular tachycardia (torsades de pointes) that occurs in the setting of a long QT
interval differs from that of other forms of ventricular
tachycardia. Class Ia or III antiarrhythmics, which prolong
the QT interval, should be avoided—or withdrawn immediately if being used in patients with long QT syndrome.
Intravenous beta-blockers may be effective in treating
electrical storm due to long QT syndrome or catecholaminergic polymorphic ventricular tachycardia. Increasing
the heart rate, whether by infusion of beta-agonist (dopamine or isoproterenol) or temporary atrial or ventricular
pacing, is an effective approach that can both break and
prevent the rhythm.
Long-term treatment of patients with inherited arrhythmia syndromes depends on the presence of high-risk features. Use of beta-blockers (particularly propranolol or
nadolol) is the mainstay of treatment for patients with long
QT syndrome or catecholaminergic polymorphic ventricular tachycardia. Surgical cervicothoracic sympathectomy
should be considered for patients who do not respond to or
are intolerant of beta-blockers. There is no reliable medication therapy for Brugada syndrome and prevention of
arrhythmias focuses on prompt treatment of exacerbating
triggers, particularly fever. Antiarrhythmic medications
should be avoided in patients with inherited arrhythmia
syndromes except for specific identified genetic abnormalities under the direction of a specialist. ICD implantation is generally recommended for patients with an
inherited arrhythmia syndrome in whom sudden cardiac
arrest is the initial presentation. An ICD should be considered in patients with recurrent sustained ventricular
arrhythmias or syncope despite medical therapy.
» When to Refer
Any patient with known or suspected inherited arrhythmia
syndrome or with severe corrected QT interval prolongation (greater than 500 msec on serial ECGs) should be
referred to a cardiologist or cardiac electrophysiologist.
Stiles MK et al. 2020 APHRS/HRS expert consensus statement
on the investigation of decedents with sudden unexplained
death and patients with sudden cardiac arrest, and of their
families. Heart Rhythm. 2021;18:e1. [PMID: 33091602]
SYNCOPE
ESSENTIALS OF DIAGNOSIS
»
Transient loss of consciousness and postural tone
from vasodepressor or cardiogenic causes with
prompt recovery without resuscitative measures.
»
High-risk features include history of structural
heart disease, abnormal ECG, and age greater
than 60 years.
» General Considerations
Syncope is a symptom defined as a transient, self-limited
loss of consciousness, usually leading to a fall. Thirty percent of the adult population will experience at least one
episode of syncope. It accounts for approximately 3% of
emergency department visits. A specific cause of syncope is
identified in about half of cases during the initial evaluation. The prognosis is relatively favorable except when
accompanying cardiac disease is present. In many patients
with recurrent syncope or near syncope, arrhythmias are
not the cause. This is particularly true when the patient has
no evidence of associated heart disease by history, examination, standard ECG, or noninvasive testing. The history
is the most important component of the evaluation to
identify the cause of syncope.
Reflex (neurally mediated) syncope may be due to
excessive vagal tone or impaired reflex control of the
peripheral circulation. The most frequent type is vasovagal
syncope or the “common faint,” which is often initiated by
a stressful, painful, or claustrophobic experience. Enhanced
vagal tone with resulting hypotension is the cause of syncope in carotid sinus hypersensitivity and postmicturi-
tion syncope; vagal-induced sinus bradycardia, sinus
arrest, and AV block are common accompaniments and
may themselves be the cause of syncope.
Orthostatic (postural) hypotension is another common cause of vasodepressor syncope, especially in older
adult patients; in patients with diabetes or others with
autonomic neuropathy; in patients with blood loss or
hypovolemia; and in patients taking vasodilators, diuretics,
and adrenergic-blocking medications. In addition, a syndrome of chronic idiopathic orthostatic hypotension
exists primarily in older men. In most of these conditions,
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