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INTRODUCTION 

— Clinicians in many disciplines commonly face the problem of evaluating and treating patients with
cardiac arrhythmias (table 1). Carefully performed randomized trials, technological advances, and better understanding of
arrhythmia mechanisms have resulted in improved approaches to rhythm disturbances. Basic evaluation and management
principles are key to the initial approach to the patient with an arrhythmia.

There are three reasons to evaluate and treat arrhythmias:

 • Eliminate symptoms.

 • Prevent imminent death and hemodynamic collapse due to a life-threatening arrhythmia.

 • Reduce possible risks other than the direct effects of the arrhythmia (eg, reduce stroke in patients with atrial fibrillation).

This topic will provide an overview of early diagnosis and management of rhythm disturbances in patients who present to
by primary care physicians. The reader will be referred to detailed discussions of the individual arrhythmias. The role of the
primary care physician in the evaluation of palpitations is discussed separately. (See "Overview of palpitations in adults".)

DEFINITION — An arrhythmia is any rhythm that is not normal sinus rhythm with normal atrioventricular (AV) conduction.
Normal sinus rhythm originates from the sinus node in the upper portion of the right atrium. During sinus rhythm, the heart
rate is in the normal range, the P waves are normal on the ECG, and the rate is stable.

The normal sinus rate has been considered to be between 60 and 100 beats/min. However, the range (defined by 2
standard deviations from the mean) is between 43 and 93 beats/min in men and 52 and 94 beats/min for women. Sinus
bradycardia or tachycardia may be physiologic (ie, normal) or nonphysiologic (ie, abnormal); each is discussed separately.
(See "Sinus bradycardia" and "Sinus tachycardia".)

Sinus arrhythmia — Not uncommonly the activation rate of the sinus node varies, leading to a variable P-P interval on the
ECG. If the variation of the P-P interval is 0.12 sec (120 msec) or more in the presence of normal P waves, this is known as
sinus arrhythmia. Sinus arrhythmia is usually physiologic and is related to respiratory cycles. It does not require treatment.
(See 'Sinus arrhythmia' above and "Normal sinus rhythm and sinus arrhythmia" and "Etiology of atrioventricular block".)

COMMON ARRHYTHMIAS — Common arrhythmias encountered in an office-based setting include:

 • Atrial premature beats (APBs)

 • Ventricular premature beats (VPBs) (figure 1)

 • Bradycardias (figure 2), including sinus bradycardia (figure 2 and table 2)

 • Ventricular Tachycardia (figure 3A-B)

 • Atrial fibrillation (AF) and atrial flutter (figure 4A-B)

 • Supraventricular tachyarrhythmias (SVTs) (figure 5 and figure 6)

 • Atrioventricular (AV) block (figure 7)

 • Nonsustained ventricular tachycardia (NSVT) (figure 8)

 • Follow-up of already treated VT or ventricular fibrillation (VF)

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The diagnosis of these arrhythmias may be difficult, even for an experienced specialist in rhythm disturbances. As an
example, the etiology of wide or narrow QRS tachycardias may be difficult based upon the electrocardiogram (ECG); an
electrophysiology study is occasionally indicated. (See "Approach to the diagnosis and treatment of wide QRS complex
tachycardias" and "Approach to the diagnosis of narrow QRS complex tachycardias".)

Some rhythm disturbances, such as symptomatic bradycardia (with syncope or near syncope) or sustained ventricular
tachycardia, require urgent attention. Others, such as ectopic atrial and ventricular beats, may cause concern but do not
need immediate management.

APPROACH TO THE PATIENT — Patients typically seek medical care for symptoms associated with an arrhythmia. They may
also request or require evaluation if there are other abnormalities that place a patient at risk for an arrhythmia, such as a
delta wave or a long QT interval on an electrocardiogram, or hypertrophic cardiomyopathy seen by an echocardiogram.
Occasionally, an asymptomatic patient who has an irregular pulse on examination, or who has an ECG, ambulatory monitor,
or exercise test for another reason is found to have an arrhythmia or evidence that may indicate an arrhythmia may be
present.

When the primary care physician first encounters a patient with an arrhythmia, the following questions should be
addressed:

 • Is the arrhythmia causing symptoms or could it?

 • Does the arrhythmia pose a risk to the patient?

 • Which arrhythmia is present?

 • Does the arrhythmia require emergent cardioversion?

 • Does the patient require urgent hospitalization?

 • Is specialist consultation required, and if so, how urgently?

 • Should anticoagulation and/or other medical therapy be started?

The initial evaluation of the patient with an arrhythmia consists of a complete history (aimed toward symptoms and timing
of the arrhythmia and potential underlying diseases), physical examination and 12-lead ECG, if possible, during the
arrhythmia and without it. The ECG alone during the arrhythmia may determine the type of arrhythmia and whether a
particular symptom is due to the arrhythmia.

Symptoms — The presence of symptoms may determine whether any action needs to be taken.

Symptoms caused by cardiac arrhythmias can mimic those due to other medical disorders and include palpitations,
dizziness, lightheadedness, syncope, chest discomfort, neck discomfort, dyspnea, weakness, and anxiety. Secondary
consequences of arrhythmias, often due to underlying heart disease, are an additional source of symptoms (eg, congestive
heart failure, ischemia, and thromboemboli.) Arrhythmias such as ventricular fibrillation and asystole can cause cardiac
arrest.

Cardiac arrhythmias can have unusual symptomatic presentations such as tinnitus, visual changes, increased urinary
frequency, abdominal discomfort, and peripheral edema. Arrhythmias may cause a change in sympathetic and vagal tone,
hormonal changes, elevation of venous pressure, and reduced cardiac output, all of which can lead to an even longer list of
other symptoms.
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Symptom type and severity are related to the etiology and rate of the arrhythmia, to the nature and severity of underlying
heart disease, and to the patient. The symptom severity often dictates the urgency for therapy or even the need to evaluate
and treat. The presence of structural heart disease is a key issue that determines the urgency of intervention, evaluation,
therapy, and the prognostic importance of the arrhythmia.

Arrhythmias commonly cause palpitations. The approach to the patient who presents with palpitations is found elsewhere.
(See "Overview of palpitations in adults".)

Diagnosis — While the history and physical exam may strongly suggest the diagnosis, such as in a patient with
lightheadedness and a rapid and irregularly irregular pulse (atrial fibrillation), the diagnosis is best made with an
electrocardiogram or a monitor. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias" and
"ECG tutorial: Atrioventricular block" and "ECG tutorial: Basic principles of ECG analysis" and "ECG tutorial: Intraventricular
block" and "ECG tutorial: Rhythms and arrhythmias of the sinus node" and "ECG tutorial: Ventricular arrhythmias".)

Many patients with a suspected arrhythmia have a paroxysmal pattern, so that the ECG recorded in the absence of
symptoms is either normal or does not suggest a specific arrhythmia. Four types of outpatient monitoring systems are
available:

 • Traditional Holter-continuous recording of 24 or 48 hours.

 • Event recorder-patient activated recorder, either looping or nonlooping. Some newer models have automatic arrhythmia
detection software to store asymptomatic episodes. Data is transmitted over the phone to a monitoring station.

 • Mobile continuous outpatient cardiac telemetry-continuous recording and analysis, with symptomatic or algorithm
defined episodes transmitted automatically via cellular technology to monitoring station.

 • Implantable loop recorder-patient and algorithm defined episodes stored in device, until interrogated either in office or
remotely via home equipment and internet.

The 1999 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on ambulatory
electrocardiography concluded that there were two main indications for ambulatory monitoring in the assessment of
arrhythmia [1]. (See "Ambulatory monitoring in the assessment of cardiac arrhythmias".)

 • For the assessment of unexplained syncope, near syncope, or episodic dizziness

 • For the assessment of unexplained recurrent palpitations

An event recorder or transtelephonic monitor can help make the diagnosis in a patient with less frequent palpitations [2].
Transtelephonic ECG devices exist in several forms of recorders and transmitters capable of direct transmission of an
electrocardiogram as an audio signal by telephone. These ECG signals are most commonly received at a base station
equipped with a demodulator and an ECG strip chart recorder. Although such devices usually provide limited,
noncontinuous sample ECG data, the device may be used in either a noncontinuous or continuous format.

Noncontinuously applied transtelephonic devices with memory are small (beeper size), lightweight instruments that are
generally inexpensive. These devices are carried by the patient; they can be applied with temporary contact to the
precordial area, or are attached by electrodes and worn continuously. The memory feature allows recording of data without
the need for immediate access to telephone transmission.

The latest innovation of transtelephonic monitoring uses a readily available wrist recorder whose circuitry is completed by
contact of the index finger and thumb, or hand contact to the opposite wrist. This action results in the loop storage of a four
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to five minute ECG sample of lead I, and permits direct printout or transtelephonic transmission. The stored data may be
transmitted by telephone directly to a facsimile machine. An implantable monitor (Reveal, Medtronic, Minneapolis, USA) is
available in Europe and will be available soon in the United States. (See "Ambulatory monitoring in the assessment of
cardiac arrhythmias".)

If episodes are associated with exercise or physical or mental stress or when an arrhythmia cannot be documented with
ambulatory or transtelephonic monitoring, a treadmill or bicycle ergometer may be helpful to establish the presence and
mechanism of the arrhythmia.

In some instances, such as in selected patients with unexplained syncope, an implantable loop recorder may be indicated to
detect the arrhythmia that may be responsible for patient symptoms. (See "Ambulatory monitoring in the assessment of
cardiac arrhythmias", section on 'Implantable loop recorder'.)

Patients presenting with an arrhythmia — Asymptomatic arrhythmias rarely require urgent treatment. In such patients, a
physician may choose to refer the patient on an elective basis to a cardiologist or cardiac electrophsyiologist.

For patients who are symptomatic in the office, the management strategy will depend both on the characteristics of the
symptoms and the type of arrhythmia present. In the following clinical scenarios, we recommend urgent transfer to a
facility with emergency care capabilities:

 • Syncope or near syncope in patients with high degree AV block or bradycardia

 • Wide complex sustained rhythms (other than sinus with bundle branch block) including ventricular tachycardia

 • Patients in whom the diagnosis is uncertain after examination and ECG, but for whom there is a concern about a life
threatening arrhythmia

 • Patients with a history of coronary artery disease, cardiomyopathy, or heart failure and syncope, near syncope, and/or
documented ventricular arrhythmia

 • Sustained supraventricular tachycardia (SVT)

 • Atrial fibrillation or flutter with rapid or slow rates

Emergent cardioversion is not indicated for any conscious patient, including those with ventricular tachycardia.

Referral to a specialist — Arrhythmias such as isolated APBs or VPBs, or atrial fibrillation are common in the general
population and many primary care physicians are comfortable and capable of managing patients with these. We suggest
elective referral to a cardiologist for the following patients:

 • Any patient with an arrhythmia when the primary care physician is uncomfortable with either diagnosis or management

 • Candidates for permanent pacing

 • Those with an uncertain diagnosis, prognosis, or management strategy

 • Those who might benefit from implantation of an implantable cardioverter defibrillator or biventricular pacemaker

 • Those who might benefit from a catheter ablation procedure

 • Those who might benefit from antiarrhythmic drug therapy

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THERAPEUTIC CONSIDERATIONS — The goal of therapy for any arrhythmia is to improve symptoms and to prevent a
potentially serious outcome, primarily a life-threatening arrhythmia and sudden death. Stroke prevention in patients with
atrial fibrillation and atrial flutter is also an important treatment objective. The decision to initiate a long-term treatment
strategy, whether it be with device or drug therapy, depends upon the severity and frequency of arrhythmia-related
symptoms compared to the risks associated with the therapy itself.

The need for long-term therapy must be carefully individualized to each patient since the severity and importance of
symptoms are highly variable. The symptoms associated with any arrhythmia can have an impact on lifestyle, occupation,
driving, and other important daily activities.

In most cases, initiation of antiarrhythmic drug therapy will be by a cardiologist or cardiac electrophysiologist. Pacemakers,
ICDs and biventricular devices are generally implanted by electrophysiologists or other physicians with special training and
certification in their placement. The ability to interrogate the devices long term is also necessary. The long-term follow-up
of patients with implanted devices also requires special training and expertise.

Antiarrhythmic drugs — We suggest the involvement of a specialist (cardiologist or electrophysiologist) when initiation of an
antiarrhythmic drug is considered. All antiarrhythmic drugs have the potential to increase ectopy or induce or aggravate
monomorphic VT, torsades de pointes, VF, conduction disturbances, or bradycardia. This phenomenon is known as
proarrhythmia (table 3). The potential for major adverse outcomes, including death, requires the expertise of a specialist
who understands the use and risks of these drugs. (See "Myocardial action potential and action of antiarrhythmic drugs".)

The risk of proarrhythmia is higher for class I drugs (table 4) in patients with structural heart disease, especially coronary
heart disease and/or left ventricular dysfunction, than in patients with structurally normal heart disease. Class II drugs (beta
blockers, except sotalol, which also has class III properties at higher dosing), have no tachyarrhythmic or proarrhythmic
effects but can cause bradycardia. Class III drugs prolong repolarization and pose the specific risk of torsades des pointes
ventricular tachycardia.

Although the exact incidence of proarrhythmia is not certain, it appears to be relatively low when antiarrhythmic drugs are
used carefully and properly. The risk varies according to the type of arrhythmia treated, the presence of structural heart
disease, the QT interval, preexisting conduction disturbances, sinus node dysfunction, patient age, the presence of heart
failure, and left and right ventricular function. The proarrhythmic risk is highest in patients with depressed left ventricular
function (eg, EF <0.30), the group at highest risk for an arrhythmic event and sudden death; the risk is lowest in those with
no organic heart disease.

Proarrhythmia can be predictable and is most often idiosyncratic. However, it may be dose-related for specific drugs,
including sotalol, class IC drugs, and the metabolite of procainamide, N-acetyl procainamide.

Torsades de pointes is the most recognized form of drug proarrhythmia. It is characterized by a VT with a twisting of the
peaks of the QRS complexes across an imaginary isoelectric line (figure 9A-C). The QT interval is prolonged, bradycardia is
often present, and the arrhythmia is induced after a short-long cycle. Torsades de pointes was originally recognized as a
complication of quinidine use, being the mechanism for "quinidine syncope". Many nonantiarrhythmic drugs including some
antibiotics, antipsychotics, and other classes of drugs, can increase the risk of torsades de pointes via prolongation of the QT
interval (table 5). (See "Acquired long QT syndrome".)

Initiation of therapy — Therapy with some (but not all) antiarrhythmic drugs is best initiated in the hospital, primarily to
monitor for early proarrhythmia. The decision to hospitalize depends upon several factors:

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 • The presence and severity of structural heart disease.

 • The indication for treatment (eg, etiology of the arrhythmia and type and severity of associated symptoms). Treatment
for ventricular tachycardia is usually started in the hospital.

 • The drug used. For example, the labeling information for dofetilide and sotalol specify inpatient initiation, while
flecainide, propafenone, dronedarone, and amiodarone can generally be initiated outside the hospital in appropriate
patients.

Following the initiation of an antiarrhythmic drug, patients should have periodic monitoring with an ECG and laboratory
tests. The frequency of such tests is higher at the time of initiation and dose adjustment. Careful monitoring of electrolytes
may help reduce the risk of proarrhythmia. Assessment of renal and/or hepatic function is also important depending on the
agent(s) being used. These drugs may interact with other drugs, which also require monitoring (for example,
amiodarone tends to increase the International Normalized Ratio (INR) and digoxin level)

 • Patients taking amiodarone should have assessment of hepatic, thyroid, and pulmonary function on a regular basis, or
with any symptoms that suggest possible organ toxicity. Patients taking amiodarone should also be cautioned regarding skin
photosensitivity. (See "Clinical use of amiodarone", section on 'Side effects'.)

SPECIFIC ARRHYTHMIAS

Atrial fibrillation and flutter — The preceding discussion has emphasized the symptoms (eg, palpitations, syncope) and life-
threatening potential of an arrhythmia itself. AF and flutter are associated with additional issues, each of which must be
addressed.

 • Reversion to sinus rhythm

 • Maintenance of sinus rhythm

 • Slowing the ventricular rate in chronic or paroxysmal atrial fibrillation

 • Prevention of systemic embolization and stroke, both at the time of reversion and in patients chronically

These issues are discussed in detail separately. (See "Overview of the evaluation and management of atrial fibrillation".)

Atrial premature beats — An atrial premature beat (APB) is the early activation of the atria arising from a site other than the
sinus node. APBs are observed on the surface electrocardiogram as a P wave that occurs relatively early in the cardiac cycle
(ie, prematurely before the next sinus P wave should occur) and has a different morphology from the sinus P wave. Often
the PR interval is different from that during sinus rhythm; it may be longer or shorter, depending upon the site of origin of
the APB. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias".)

APBs may be asymptomatic or cause symptoms such as a sensation of "skipping" or palpitations. APBs are often single and
isolated, but may be frequent and may occur in a bigeminal or other repeated pattern. A trigger/stimulant is often identified
and its removal may eliminate or significantly reduce symptoms. Antiarrhythmic drug therapy, aside from beta blockers, is
rarely recommended. (See "Supraventricular premature beats".)

APB's may be blocked in the A-V conducting system. This is not necessarily pathologic, and it needs to be differentiated
from atrioventricular block.

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Ventricular premature beats — Ventricular premature beats (VPBs) are common in the general population and often cause
patients to seek medical attention. This includes patients without structural heart disease and those with any form of
cardiac disease, independent of severity. The evaluation and management of VPBs is discussed elsewhere. (See "Prevalence
and evaluation of ventricular premature beats" and "Clinical significance and treatment of ventricular premature beats".)
and see

"Role of antiarrhythmic drugs for ventricular arrhythmias in patients with a prior myocardial infarction").

ARRHYTHMIA IN ATHLETES — Arrhythmias are not infrequently documented in athletes and can be a source of morbidity
and mortality, particularly ventricular tachyarrhythmia and sudden cardiac arrest. They can be a reason to consider
restriction from athletics. (See "Overview of sudden cardiac arrest and sudden cardiac death".)

The evaluation and management of arrhythmia in athletes is discussed separately. (See "Arrhythmia in athletes".)

ROLE OF THE PCP IN LONG-TERM CARE — The role of the PCP in the long-term care of patients with arrhythmias depends
upon the particular arrhythmia diagnosis and treatment. All patients should be queried at each routine visit about changes
in symptoms relevant to the arrhythmia and its treatment.

Patients with pacemakers, implantable cardioverter defibrillators, or cardiac resynchronization therapy implantation are
best followed periodically and evaluated by physicians knowledgeable in device programming, device characteristics, and
their possible malfunction.

Patients prescribed antiarrhythmic drug therapy are generally followed by a cardiologist and/or cardiac electrophysiologist.

SUMMARY — An arrhythmia is any rhythm that is not normal sinus rhythm with normal atrioventricular (AV) conduction.
Normal sinus rhythm originates from the sinus node in the upper portion of the right atrium. During sinus rhythm, the heart
rate is in the normal range, the P waves are normal on the ECG, and the rate is stable. (See 'Definition' above.)

When the primary care clinician first encounters a patient with an arrhythmia, the following questions should be addressed
(see 'Approach to the patient' above:

 • Is the arrhythmia causing symptoms or could it?

 • Does the arrhythmia pose a risk to the patient?

 • Which arrhythmia is present?

 • Does the arrhythmia require emergent cardioversion?

 • Does the patient require urgent hospitalization?

 • Is specialist consultation required, and if so, how urgently?

 • Should anticoagulation and/or other medical therapy be started?

For patients who are symptomatic in the office, the management strategy will depend both on the characteristics of the
symptoms and the type of arrhythmia present. In the following clinical scenarios, we recommend urgent transfer to a
facility with emergency care capabilities (see 'Patients presenting with an arrhythmia' above:

 • Syncope or near syncope in patients with high degree AV block or bradycardia

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 • Wide complex rhythms (other than sinus with bundle branch block) including ventricular tachycardia

 • Patients in whom the diagnosis is uncertain after examination and ECG, but for whom there is a concern about a life
threatening arrhythmia

 • Patients with a history of coronary artery disease, cardiomyopathy, or heart failure and syncope, near syncope, and/or
documented ventricular arrhythmia

 • Sustained supraventricular tachycardia (SVT)

 • Atrial fibrillation or flutter with rapid or slow rates

All antiarrhythmic drugs have the potential to increase ectopy or induce or aggravate monomorphic VT, torsades de
pointes, VF, conduction disturbances, or bradycardia; this known as proarrhythmia (table 3). We suggest the involvement of
a specialist (cardiologist or electrophysiologist) when initiation of an antiarrhythmic drug is considered. (See 'Initiation of
therapy' above.)

The role of the PCP in the long-term care of patients with arrhythmias depends upon the particular arrhythmia diagnosis
and treatment. All patients should be queried at each routine visit about changes in symptoms relevant to the arrhythmia
and its treatment.

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