Official reprint from UpToDate®

www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Multifocal atrial tachycardia

Author: Alfred Buxton, MD

Section Editor: Leonard I Ganz, MD, FHRS, FACC
Deputy Editor: Brian C Downey, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Oct 12, 2017.

INTRODUCTION — Multifocal atrial tachycardia (MAT) is an arrhythmia that can be seen in a variety
of clinical disorders [1]. In addition to a heart rate greater than 100 beats per minute, the characteristic
electrocardiographic feature is variability in P wave morphology, with each unique P wave morphology
felt to indicate a different site of atrial origin. Although this abnormality had been noted for many years
during some types of atrial tachycardia, the term MAT became commonplace terminology in the late
1960s [2]. Patients with multiple P wave morphologies but a normal heart rate (60 to 100 beats per
minute) are considered to have a wandering atrial pacemaker, since the heart rate does not meet
criteria for a tachycardia. (See 'Terminology' below.)

This topic will review the definition, pathogenesis, etiology, and treatment of MAT in adults. Other
tachycardias of atrial origin, as well as the discussion of this arrhythmia in children, are reviewed
separately. (See "Focal atrial tachycardia" and "Atrial tachycardias in children" and "Atrioventricular
nodal reentrant tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an
accessory pathway" and "Overview of atrial fibrillation".)

DEFINITION, PATHOGENESIS, AND PREVALENCE — As with any tachycardia, the heart rate in
MAT exceeds 100 beats per minute. To distinguish MAT from other tachyarrhythmias of atrial origin,
there should be organized atrial activity yielding P waves with three or more different morphologies.
(See 'Clinical manifestations and diagnosis' below.)

Terminology — A number of authors have used the term "chaotic" to describe MAT [3-5]. However,
chaos in modern usage in nonlinear dynamics and mathematics implies there is order in what appear
to be random events [6]. A more accurate term for this arrhythmia is probably "multiform" as there is
no proof that the arrhythmia is actually multifocal, although multifocal remains the commonly used
term [1].

The tachycardic threshold for multifocal atrial tachycardia (MAT) has traditionally been set at 100 bpm,
but a review of 60 patients with multifocal atrial arrhythmias found a stronger association between the
incidence of COPD exacerbations and the diagnosis of MAT if a threshold of 90 bpm was used [7].
Some patients have similar electrocardiographic (ECG) findings with multiple P wave morphologies
but do not meet criteria for tachycardia. The arrhythmia is called a multifocal atrial rhythm or
wandering atrial pacemaker if the rate is between 60 and 100 beats per minute. A distinction has been
made between the two based on the clinical picture, with a wandering atrial pacemaker usually
occurring in the asymptomatic or less ill individual [1].

Mechanisms — The changing morphology of the P waves and the variable PR interval suggests that
the atrial pacemaker activity arises from different atrial locations. However, the variable PR interval is
probably more likely a result of the variable atrial rate. Alternatively, a single focus with different exit
pathways or abnormalities in intraatrial conduction could produce the identical electrocardiographic
findings. There have only been a few invasive electrophysiologic investigations of MAT, but one study
did show abnormal intraatrial, atrionodal, and atrioventricular nodal conduction in many individuals
with MAT [5]. One case report demonstrated origin of multiform atrial premature complexes from
adjacent areas in the right pulmonary veins [8]. However, this patient did not have the typical setting in
which MAT is seen.

Automaticity refers to normal, accelerated normal, or abnormal pacemaker activity. Triggered activity,
on the other hand, results from a normal stimulus giving rise to afterdepolarization, which, if threshold
is attained, can result in regenerative action potentials (resulting in tachycardia) in any cardiac tissue.
Reentry refers to a circuit in which previously excited tissue is re-excited, producing an extra beat or a
sustained rhythm. The occasional responsiveness of MAT to verapamil suggests intracellular calcium
overload causing afterdepolarizations leading to triggered activity as the underlying mechanism [9,10].

It is thought that MAT results from right atrial hypertension and distension, either from secondary
pulmonary hypertension from advanced COPD or left ventricular dysfunction caused by comorbid
processes such as coronary heart disease, systemic hypertension, or aortic stenosis [11,12]. However,
although frequently associated with exacerbations of pulmonary disease, MAT may occur in other
circumstances, so atrial distension may not be a universal mechanism.

Associated arrhythmias — MAT (and wandering atrial pacemaker) is commonly accompanied by

atrial premature beats and can itself be considered a prolonged sequence of atrial premature beats
[1]. The majority of episodes of MAT are self-limited and non-sustained.

MAT may be associated with or precede atrial fibrillation [2,13]. In one report of 31 patients, for
example, 55 percent developed atrial fibrillation or flutter [14].

Prevalence — MAT is an uncommon but not rare arrhythmia. It has been estimated to occur in 0.05 to
0.32 percent of electrocardiograms in general hospitals and in 0.37 percent of hospitalized patients
[1,2]. The average age is approximately 70 years. These elderly patients are generally quite ill, with an
in-hospital mortality rate of 40 to 60 percent due to pulmonary, cardiac, and other serious diseases.

ASSOCIATED CLINICAL CONDITIONS

Pulmonary disease — MAT is associated with significant lung disease in roughly 60 percent of cases
[1,15]. Furthermore, this arrhythmia has been identified in up to 20 percent of patients hospitalized for
acute respiratory failure [16]. COPD is the most common pulmonary disorder associated with MAT, but
this arrhythmia can also occur with pneumonia and pulmonary embolism. Hypoxia, hypercapnia,
acidosis, autonomic imbalance, right atrial enlargement, and therapy with aminophylline, theophylline,
or isoproterenol all may contribute to the enhanced ectopic atrial activity [2,9,17]. (See "Arrhythmias in
COPD".)

Cardiac disease — MAT can occur in the presence of coronary, valvular, hypertensive and other
types of heart disease, particularly when associated with heart failure and/or underlying lung disease.
Affected patients tend to have elevated pulmonary capillary wedge and pulmonary end-diastolic
pressures as well as a low-normal cardiac index [18]. [2,13].

Interactions between cardiac and pulmonary disease — In advanced cases of cardiac and
pulmonary disease, MAT may be part of a complicated pathophysiologic complex in which several
conditions (eg, pulmonary hypertension, elevated left ventricular filling pressures, and MAT) contribute
to the progression and persistence of each other [12,19,20]. Illustrations of these relationships include:

● Severe pulmonary arterial hypertension has been associated with and may cause LV diastolic
dysfunction [19,20]. (See "Pulmonary hypertension in patients with left heart failure" and
"Classification and prognosis of pulmonary hypertension in adults" and "Clinical manifestations
and diagnosis of heart failure with preserved ejection fraction".)

● Theoretically, the rapid heart rate associated with MAT decreases diastolic filling time and can
result in increased LV diastolic pressure, which in turn increases pulmonary artery pressure that
encourages MAT [12]. However, the vast majority of episodes of MAT are brief and not associated
with symptoms or recognizable hemodynamic compromise. (See "Clinical manifestations and
diagnosis of heart failure with preserved ejection fraction".)

● Prolonged episodes of tachycardia can cause a cardiomyopathy. (See "Arrhythmia-induced

cardiomyopathy".)

Miscellaneous — MAT is also associated with a number of other disorders:

● Hypokalemia – MAT has been associated with hypokalemia, most often induced by diuretic use
[1-3]. Hypokalemia may predispose to MAT by increasing the rate of phase 4 depolarization
(figure 1) in atrial tissues. (See "Clinical manifestations and treatment of hypokalemia in adults",
section on 'Cardiac arrhythmias and ECG abnormalities'.)

● Hypomagnesemia – The administration of magnesium can suppress MAT in hypomagnesemic

and, at times, in apparently normomagnesemic patients [21]. (See "Clinical manifestations of
magnesium depletion".)

● Drugs – As noted above, isoproterenol, aminophylline, and theophylline can induce or exacerbate
MAT, particularly in the presence of pulmonary disease [2,9,17]. By comparison, digitalis is
generally not considered to be a cause of MAT, although some reports suggest that such an
association may exist [2,3,13,14,22,23].

● Chronic renal failure – Approximately 15 percent of patients with MAT have chronic renal failure
[3,22]. It is unclear, however, if this represents a cause-and-effect relationship.

● Other – MAT also can occur in sepsis and after recent surgery, particularly if the patient has
pulmonary compromise and/or heart failure [1,2].
MAT in children and young adults — The association of MAT with serious illness is generally less in
children than in adults. Information on multifocal (or chaotic) atrial tachycardia in children is presented
separately. (See "Atrial tachycardias in children", section on 'Chaotic atrial tachycardia'.)

CLINICAL MANIFESTATIONS AND DIAGNOSIS

Clinical manifestations — In most cases, the clinical manifestations of MAT differ from those of other
tachyarrhythmias in that symptoms predominantly relate to the underlying precipitating illness rather
than the arrhythmia [15]. Patients have an irregular heart rate greater than 100 beats per minute. The
arrhythmia is usually recognized only by ECG monitoring, as the majority of patients are acutely ill and
on continuous ECG monitoring. Patients rarely present with symptoms such as palpitations.
Presyncope or syncope is generally not associated with this arrhythmia. Given that the majority of
patients with MAT are concurrently affected by advanced or decompensated pulmonary disease,
many patients have typical symptoms related to the underlying lung disease (eg, shortness of breath,
wheezing, productive cough, etc) or acute metabolic derangements.

Most episodes of MAT do not precipitate hemodynamic compromise or limiting symptoms [15].
However, higher heart rates associated with MAT can sometimes worsen systemic oxygenation in
patients with advanced pulmonary disease. Additionally, in patients with coexistent advanced cardiac
disease, namely those with severe multivessel obstructive coronary artery disease or decompensated
heart failure, the faster heart rates associated with MAT can exacerbate heart disease, leading to
signs and symptoms of cardiac decompensation (eg, angina, dyspnea, orthopnea). Symptomatic
decompensation of underlying cardiac or pulmonary disease is an indication for pharmacologic
therapy aimed specifically at the tachycardia rather than therapy to control the underlying disease
process. (See 'Pharmacologic therapy' below.)

Diagnosis — The diagnosis of MAT can be suspected from the presence of an irregular rapid pulse
and heartbeat on physical examination, usually in a patient with underlying, often poorly controlled,
cardiac or pulmonary disease. The diagnosis cannot be confirmed, however, without an
electrocardiogram (ECG).

A diagnosis of MAT requires the following be present on the ECG (waveform 1) [1,2]:

● Discrete P waves with at least three different morphologies (including the normal sinus P wave).

● An atrial rate greater than 100 beats per minute, which is the classic definition of MAT [2].
However, based upon data from a series of patients with chronic obstructive pulmonary disease
(COPD), a threshold of 90 bpm has been proposed [7].

● P waves which return to the baseline and thus are separated by isoelectric intervals.

● P-P intervals, P-R duration, and R-R intervals which vary.

Differential diagnosis — The differential diagnosis for MAT is similar to that of other narrow QRS
complex tachycardias with an irregular rhythm (assuming there is normal AV conduction without
bundle branch block) and includes:

● Sinus tachycardia with frequent atrial premature beats (APBs) or ventricular premature beats
(VPBs)
 ● Atrial tachycardias (including atrial flutter) with variable AV conduction
● Atrial fibrillation

MAT can usually be differentiated from both atrial flutter with variable AV conduction and sinus
tachycardia with APBs/VPBs by the regular P-P interval seen in both atrial flutter and sinus
tachycardia, which is not present in MAT. (See "Electrocardiographic and electrophysiologic features
of atrial flutter", section on 'Electrocardiographic features'.)

MAT, with its organized atrial activity resulting in P waves on surface ECG, can be readily
distinguished from atrial fibrillation, which lacks any discernible P waves. However, MAT can and does
degenerate into atrial fibrillation in some patients. (See "The electrocardiogram in atrial fibrillation".)

A more in-depth discussion of the differential diagnosis of narrow QRS complex tachycardias is
presented separately. (See "Clinical manifestations, diagnosis, and evaluation of narrow QRS complex
tachycardias".)

TREATMENT — Most episodes of MAT do not precipitate hemodynamic compromise or symptoms.

Thus, therapy in patients with MAT should be aimed at the inciting underlying disease [15,24].
Amelioration of MAT generally parallels improvement in severe pulmonary or cardiac disease or
sepsis. Not infrequently, medication used for the treatment of pulmonary disease, such as
theophylline, induces or exacerbates MAT [2,9,17]. In many cases, MAT is precipitated by poor
oxygenation and/or acid-base disturbances.

In addition to treatment for the underlying pathologic condition associated with MAT, specific therapies
for the tachycardia are sometimes used (usually only if the arrhythmia is so frequent or sustained as to
compromise oxygenation or cause hemodynamic compromise). In patients with electrolyte
disturbances, maintaining magnesium and potassium levels in the normal range is important.
Pharmacologic therapy to slow the ventricular heart rate, using either verapamil or a beta blocker, is
administered for patients with signs or symptoms felt to be related to their tachycardia. While rate
control therapy is often very effective, there is no role for electrical cardioversion or antiarrhythmic
drug therapy in patients with MAT.

Magnesium and potassium repletion — Patients with MAT and associated hypokalemia or
hypomagnesemia should undergo electrolyte repletion prior to the initiation of additional medical
therapy for MAT [24].

Hypomagnesemia appears to promote the development of some atrial and ventricular arrhythmias.
The administration of magnesium has been reported to suppress MAT in the hypomagnesemic patient
and, at times, in patients with normal plasma magnesium levels [21,25]. As an example, one study
randomized 14 patients with chronic obstructive pulmonary disease and MAT to magnesium therapy
(2 grams over 5 minutes and 10 grams over 5 hours) or placebo [25]. At 5 hours, patients treated with
magnesium had a slowing of heart rate from 130 to 99 beats per minute, while there was no change in
the placebo group. Sinus rhythm was present at the end of the infusion in 7 of 9 patients treated with
magnesium versus one of five receiving placebo. (See "Clinical manifestations of magnesium
depletion".)

Mild hypomagnesemia (serum magnesium 1.4 to 1.7 mg/dL) can be treated with 240 mg of elemental
magnesium orally twice per day as magnesium oxide (400 mg twice daily) or a delayed release
magnesium chloride preparation. Dose-dependent diarrhea occurs frequently. More significant
hypomagnesemia (serum magnesium <1.4 mg/dL) can be treated with 1 gram (8 mEq) of magnesium
sulfate given intravenously over 15 minutes, followed by a continuous infusion of 3 to 6 grams (24 to
48 mEq) over 24 hours, OR as repeated intermittent infusions, each consisting of 1 gram over 1 hour,
for a total of 3 to 6 grams over 12 hours. Because magnesium distributes gradually to tissues, early
serum levels can appear artificially high, and repletion may require several days of treatment. The
dose should be reduced by approximately 50 percent with even mild renal insufficiency. Response to
the initial dose may give an indication of whether the MAT will be responsive to magnesium therapy.
(Conversion relationships: 1 mmol = 2 mEq = 24 mg of elemental magnesium.)

Potassium repletion in the hypokalemic patient may also control MAT, with or without magnesium
supplementation [21,26]. In an observational study of eight patients, the combined use of magnesium
and potassium was associated with conversion to sinus rhythm in seven [21].

Potassium depletion can be treated with potassium chloride given either orally (20 to 60 mEq per day
in divided doses if >40 mEq) or intravenously (generally up to 10 mEq per hour, but occasionally at an
initial rate of as much as 40 mEq per hour with severe hypokalemia with continuous echocardiogram
[ECG] monitoring). The patient's serum potassium should be carefully monitored to avoid
hyperkalemia. Over the long-term, the cause of potassium loss should also be treated, (eg, the
administration of a potassium-sparing diuretic to patients treated with loop or thiazide diuretics). (See
"Clinical manifestations and treatment of hypokalemia in adults".)

Pharmacologic therapy — The use of antiarrhythmic drugs in the treatment of MAT has generally
been disappointing [1,24]. Additionally, administration of antiarrhythmic agents to acutely ill patients
with renal and/or hepatic dysfunction increases the risk of toxic reactions to these agents. There is,
however, evidence of benefit with agents to control the ventricular heart rate, namely verapamil and
beta blockers.

Medical therapy for MAT is indicated only if MAT causes a sustained rapid ventricular response that
causes or worsens myocardial ischemia, heart failure, peripheral perfusion, or oxygenation [15,27].
For patients with symptomatic MAT requiring ventricular rate control, we recommend therapy with
verapamil or a beta blocker (table 1).

Non-dihydropyridine calcium channel blockers — While both diltiazem and verapamil can be
effective agents for slowing atrioventricular (AV) nodal conduction and controlling ventricular heart
rates, verapamil has been most commonly used in MAT, and the response in some cases suggests
that triggered activity may initiate the arrhythmia. (See 'Mechanisms' above.)

Verapamil decreases the ventricular rate by reducing the degree of atrial ectopy and/or by limiting the
transmission of beats through the AV node [1,18,28-30]. In an analysis of pooled data, verapamil
lowered the ventricular rate by an average of 31 beats per minute, but only 43 percent of patients
reverted to a sinus rhythm [1]. Furthermore, MAT may recur if verapamil is discontinued.

The following regimen, given with continuous ECG and blood pressure monitoring, has been
suggested for intravenous verapamil (table 1) [10]. A 1 mg test dose is given. The onset of action is
within 1 to 2 minutes, with a peak effect at 10 to 15 minutes. If, after 2 minutes, the dose is tolerated,
an additional 4 mg is administered over 5 minutes. If MAT persists and high-degree AV block is not
present, an additional 5 mg is given over 5 minutes. Ten mg is typically sufficient, but if the response
to the initial doses is inadequate and if verapamil has been well tolerated, one to two additional 5 mg
doses over 5 minutes at 10-minute intervals can be administered if needed. If MAT reverts to sinus
rhythm, oral verapamil is given at an initial dose of 80 mg every 6 hours and subsequently titrated as
blood pressure and heart rate allow (total daily dose range 120 to 480 mg).

Beta blockers — Beta blockers can suppress ectopic foci and decrease transmission through the
AV node, thereby slowing the ventricular response. Their use in MAT has been limited because of the
risk in patients with underlying heart failure or chronic obstructive pulmonary disease, particularly
when bronchospasm is part of the picture. However, several studies showing a benefit have been
performed, particularly with the relatively cardioselective agent metoprolol [31-33]. Esmolol and
acebutolol have also been used in small numbers of patients [34-36].

The pooled data from the metoprolol studies revealed an average decrease in ventricular rate of 51
beats per minute, with 79 percent of patients reverting to sinus rhythm [1]. Side effects were few, but
long-term therapy is required in approximately one-quarter of patients [33].

We use the following protocol for intravenous (IV) metoprolol (table 1) [32]. Five mg of metoprolol is
administered IV over 5 minutes. This can be repeated every 10 minutes for three or four doses if
tolerated (maximum IV loading dose 20 mg). In patients who are unable to receive oral medications,
subsequent doses of IV metoprolol can be administered every 4 to 6 hours with the patient in a
monitored setting. An advantage of metoprolol is the ease of switching to an oral preparation in a dose
of 50 to 100 mg twice per day. Beta blockers should generally not be given to patients with acute
decompensated heart failure, severe reactive pulmonary disease, hypotension, drug hypersensitivity,
and a history or ECG showing greater than first-degree heart block, bifascicular block, or serious sinus
node dysfunction (unless a pacemaker is implanted).

Precautions with verapamil and beta blockers — Verapamil and beta blockers should not be
given to patients with sinus node dysfunction or preexisting second- or third-degree block unless a
temporary or permanent pacemaker has been implanted. Verapamil should be administered
cautiously in patients with preexisting heart failure or hypotension as it has both negative inotropic and
peripheral vasodilator activity, potentially leading to a reduction in blood pressure or even significant
hypotension [18,28]. Beta blockers should also be administered cautiously in patients with acutely
decompensated heart failure. Verapamil and beta blockers should either be avoided or used at lower
doses and with caution in patients already treated with a beta blocker, verapamil or another calcium
channel blocker, or digoxin. (See "Major side effects of beta blockers" and "Major side effects and
safety of calcium channel blockers".)

Which to use first: Calcium channel blocker or beta blocker? — The decision to use a non-
dihydropyridine calcium channel blocker or a beta blocker is most often determined by the presence or
absence of acute decompensated heart failure with reduced left ventricular ejection fraction and
severe bronchospasm. We prefer metoprolol before verapamil in patients without these complications.
In a randomized, double-blind study of 13 patients, the incidence of benefit was 89 percent with
metoprolol versus 44 percent with verapamil [27]. (See "Use of beta blockers in heart failure with
reduced ejection fraction" and "Treatment and prognosis of heart failure with preserved ejection
fraction", section on 'Beta blockers'.)
By contrast, we prefer to begin with verapamil (or diltiazem) in patients with severe bronchospasm.
Beta blockers may be used cautiously in some patients with heart failure, but active bronchospasm is
a contraindication. (See "Use of beta blockers in heart failure with reduced ejection fraction".)

In either case, repletion of electrolyte deficiencies (hypomagnesemia and hypokalemia) should occur
simultaneously. (See 'Magnesium and potassium repletion' above.)

Antiarrhythmic drugs — For patients with symptomatic MAT that remains inadequately rate-
controlled following treatment of the underlying disorder and initiation of rate controlling therapy, we do
not use an antiarrhythmic drug. This is based on extensive literature showing a general lack of
efficacy of standard antiarrhythmic drugs in treating MAT [24]. Ineffective drugs include quinidine,
procainamide, lidocaine, and phenytoin, among others [1]. Digitalis also appears to have little benefit
[2,13].

Ibutilide has been used successfully to treat MAT in one elderly patient, but more experience with this
drug is need [37]. Additionally, ibutilide should never be used in the presence of known or suspected
hypokalemia or hypomagnesemia. (See "Therapeutic use of ibutilide".)

DC cardioversion — DC cardioversion has not proven effective in converting MAT into a sinus
rhythm [13,24,38]. As such, we do not perform cardioversion for patients with symptomatic MAT that
remains inadequately rate-controlled.

Radiofrequency ablation — Ablation of the AV node and the use of a permanent ventricular
pacemaker is an option for patients with ongoing symptomatic MAT who do not respond to, or cannot
tolerate, pharmacologic therapy. This procedure should rarely be required, because the vast majority
of MAT episodes are brief and because the arrhythmia resolves with correction of the underlying
abnormality [15]. To re-emphasize this, AV junction ablation resulting in creation of complete heart
block necessitating permanent pacemaker implantation should not be performed for the purpose of
making the ECG appear more normal. It should only be performed in order to improve
cardiopulmonary function after proving that the arrhythmia is actually the cause of hemodynamic
compromise.

Since most of the manifestations associated with MAT are due to the rapid ventricular rate, an
alternative approach for rate control is radiofrequency modification of the AV junction, similar to the
approach taken for rate control in atrial fibrillation. Ablation to cure MAT is rarely indicated and not
likely to be effective given the underlying diffuse atrial abnormalities. Early data concerning
radiofrequency modification of the AV node were encouraging, but modification of AV transmission
without producing complete heart block is unreliable and rarely long-lasting.

AV node modification with ablation was evaluated in one study of 13 patients with chronic obstructive
lung disease and medically refractory MAT who underwent AV junctional modification [39]. This
procedure resulted in adequate control of the ventricular response rate in 84 percent of patients, and
the rate was reduced from an average of 145 to 89 beats per minute. One patient developed complete
heart block, and one patient had recurrent symptomatic MAT, requiring a second procedure. After a
six-month follow-up, all patients with successful modification had an improved quality of life, a
reduction in symptoms, and an increase in left ventricular ejection fraction. (See "Control of ventricular
rate in atrial fibrillation: Nonpharmacologic therapy".)
SUMMARY AND RECOMMENDATIONS

● Multifocal atrial tachycardia (MAT) is an arrhythmia that can be seen in a variety of clinical
disorders in adults, children, and infants. In addition to a heart rate >100 beats per minute, the
characteristic electrocardiographic feature in MAT is variability in P wave morphology, with three
or more distinct P wave morphologies. (See 'Introduction' above.)

● Some patients have similar electrocardiographic (ECG) findings with multiple P wave
morphologies but do not meet criteria for tachycardia. The arrhythmia is called a multifocal atrial
rhythm or wandering atrial pacemaker if the rate is between 60 and 100 beats per minute. (See
'Terminology' above.)

● MAT is associated with significant lung disease in roughly 60 percent of cases and is identified in
up to 20 percent of patients hospitalized for acute respiratory failure. MAT can also occur in the
presence of coronary, valvular, hypertensive and other types of heart disease, particularly when
associated with heart failure and/or underlying lung disease. (See 'Associated clinical conditions'
above.)

● In most cases, the clinical manifestations of MAT differ from those of other tachyarrhythmias in
that symptoms predominantly relate to the underlying precipitating illness rather than the
arrhythmia. Patients have an irregular heart rate greater than 100 beats per minute, usually
identified only during the physical exam by the health care provider, and they rarely present with
symptoms of palpitations, presyncope, or syncope as the sole manifestation of MAT. (See 'Clinical
manifestations and diagnosis' above.)

● The diagnosis of MAT can be suspected from the presence of an irregular rapid pulse and
heartbeat on physical examination; however, the diagnosis cannot be confirmed without an ECG.
A diagnosis of MAT requires the following be present on the ECG (waveform 1) (see 'Clinical
manifestations and diagnosis' above):

• Discrete P waves with at least three different morphologies (including the normal sinus P
wave)

• An atrial rate greater than 100 beats per minute

• P waves which are separated by isoelectric intervals

• P-P intervals, P-R duration, and R-R intervals which vary

● Most episodes of MAT do not precipitate hemodynamic compromise or limiting symptoms. Thus,
therapy in patients with MAT should be aimed at the inciting underlying disease. (See 'Treatment'
above.)

● Patients with MAT and associated hypokalemia or hypomagnesemia should undergo electrolyte
repletion prior to the initiation of additional medical therapy for MAT. (See 'Magnesium and
potassium repletion' above.)

● Medical therapy for MAT is indicated only if MAT causes a sustained rapid ventricular response
that causes or worsens myocardial ischemia, heart failure, peripheral perfusion, or oxygenation.
 Options for medical therapy for patients with symptomatic MAT requiring ventricular rate control
include non-dihydropyridine calcium channel blockers and beta blockers. For patients without
heart failure or bronchospasm, we suggest initial therapy with a beta blocker, usually metoprolol,
before calcium channel blockers (Grade 2C). Conversely, for patients with severe bronchospasm,
we suggest initial therapy with a non-dihydropyridine calcium channel blocker, usually verapamil,
rather than a beta blocker (Grade 2C). Beta blockers may be used cautiously in some patients
with heart failure. (See 'Pharmacologic therapy' above.)

● Extensive literature has shown a lack of efficacy of numerous standard antiarrhythmic drugs
(including quinidine, procainamide, lidocaine, phenytoin, and digoxin) as well as electrical
cardioversion in treating MAT. (See 'Antiarrhythmic drugs' above and 'DC cardioversion' above.)

● Ablation of the AV node and the use of a permanent ventricular pacemaker is rarely indicated,
and should be reserved for patients with ongoing symptomatic MAT who do not respond to or
cannot tolerate pharmacologic therapy. (See 'Radiofrequency ablation' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Kastor JA. Multifocal atrial tachycardia. N Engl J Med 1990; 322:1713.

2. Shine KI, Kastor JA, Yurchak PM. Multifocal atrial tachycardia. Clinical and electrocardiographic
features in 32 patients. N Engl J Med 1968; 279:344.
3. Berlinerblau R, Feder W. Chaotic atrial rhythm. J Electrocardiol 1972; 5:135.
4. Bisset GS 3rd, Seigel SF, Gaum WE, Kaplan S. Chaotic atrial tachycardia in childhood. Am
Heart J 1981; 101:268.
5. Gavrilescu, S, Luca, C . Chaotic atrial rhythm: Studies with His bundle electrography. Eur J
Cardiol 1974; 2:153.
6. Glass L, Mackey MC. From Clocks to Chaos: The Rhythms of Life, Princeton University Press, P
rinceton, NJ 1988.
7. Kothari SA, Apiyasawat S, Asad N, Spodick DH. Evidence supporting a new rate threshold for
multifocal atrial tachycardia. Clin Cardiol 2005; 28:561.
8. Yokoshiki H, Mitsuyama H, Watanabe M, Tsutsui H. Swallowing-induced multifocal atrial
tachycardia originating from right pulmonary veins. J Electrocardiol 2011; 44:395.e1.
9. Marchlinski FE, Miller JM. Atrial arrhythmias exacerbated by theophylline. Response to
verapamil and evidence for triggered activity in man. Chest 1985; 88:931.
10. Levine JH, Michael JR, Guarnieri T. Treatment of multifocal atrial tachycardia with verapamil. N
Engl J Med 1985; 312:21.
11. Santos-Ocampo CD, Sadaniantz A, Elion JL, et al. Echocardiographic assessment of the cardiac
anatomy in patients with multifocal atrial tachycardia: a comparison with atrial fibrillation. Am J
Med Sci 1994; 307:264.
12. Engel TR, Radhagopalan S. Treatment of multifocal atrial tachycardia by treatment of pulmonary
insufficiency: or is it vice versa? Chest 2000; 117:7.
13. Wang K, Goldfarb BL, Gobel FL, Richman HG. Multifocal atrial tachycardia. Arch Intern Med
1977; 137:161.
14. Lipson MJ, Naimi S. Multifocal atrial tachycardia (chaotic atrial tachycardia). Clinical associations
and significance. Circulation 1970; 42:397.
15. Goudis CA, Konstantinidis AK, Ntalas IV, Korantzopoulos P. Electrocardiographic abnormalities
and cardiac arrhythmias in chronic obstructive pulmonary disease. Int J Cardiol 2015; 199:264.
16. Hudson LD, Kurt TL, Petty TL, Genton E. Arrhythmias associated with acute respiratory failure in
patients with chronic airway obstruction. Chest 1973; 63:661.
17. Levine JH, Michael JR, Guarnieri T. Multifocal atrial tachycardia: a toxic effect of theophylline.
Lancet 1985; 1:12.
18. Hazard PB, Burnett CR. Verapamil in multifocal atrial tachycardia. Hemodynamic and respiratory
changes. Chest 1987; 91:68.
19. Tutar E, Kaya A, Güleç S, et al. Echocardiographic evaluation of left ventricular diastolic function
in chronic cor pulmonale. Am J Cardiol 1999; 83:1414.
20. Moustapha A, Kaushik V, Diaz S, et al. Echocardiographic evaluation of left-ventricular diastolic
function in patients with chronic pulmonary hypertension. Cardiology 2001; 95:96.
21. Iseri LT, Fairshter RD, Hardemann JL, Brodsky MA. Magnesium and potassium therapy in
multifocal atrial tachycardia. Am Heart J 1985; 110:789.
22. Phillips J, Spano J, Burch G. Chaotic atrial mechanism. Am Heart J 1969; 78:171.
23. Chung EK. Appraisal of multifocal atrial tachycardia. Br Heart J 1971; 33:500.
24. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of
Adult Patients With Supraventricular Tachycardia: A Report of the American College of
Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart
Rhythm Society. Circulation 2016; 133:e506.
25. McCord JK, Borzak S, Davis T, Gheorghiade M. Usefulness of intravenous magnesium for
multifocal atrial tachycardia in patients with chronic obstructive pulmonary disease. Am J Cardiol
1998; 81:91.
26. Strickberger SA, Miller CB, Levine JH. Multifocal atrial tachycardia from electrolyte imbalance.
Am Heart J 1988; 115:680.
27. Parrillo, JE . Treating multifocal atrial tachycardia (MAT) in a critical care unit: New data
regarding verapamil and metoprolol. Update Crit Care Med 1987; 2:1, 3.
28. Schettini B, Katz S, Zeldis SM. Verapamil in tachycardia therapy. Chest 1986; 89:616.
29. Mukerji V, Alpert MA, Diaz-Arias M, Sanfelippo JF. Termination and suppression of multifocal
atrial tachycardia with verapamil. South Med J 1987; 80:269.
30. Salerno DM, Anderson B, Sharkey PJ, Iber C. Intravenous verapamil for treatment of multifocal
atrial tachycardia with and without calcium pretreatment. Ann Intern Med 1987; 107:623.
31. Hanau, SP, Solar, et al. Metoprolol in the treatment of multifocal atrial tachycardia. Cardiovasc
Rev Rep 1984; 5:1182.
32. Arsura EL, Solar M, Lefkin AS, et al. Metoprolol in the treatment of multifocal atrial tachycardia.
Crit Care Med 1987; 15:591.
33. Hazard PB, Burnett CR. Treatment of multifocal atrial tachycardia with metoprolol. Crit Care Med
 1987; 15:20.
34. Byrd RC, Sung RJ, Marks J, Parmley WW. Safety and efficacy of esmolol (ASL-8052: an
ultrashort-acting beta-adrenergic blocking agent) for control of ventricular rate in supraventricular
tachycardias. J Am Coll Cardiol 1984; 3:394.
35. Aronow WS, Van Camp S, Turbow M, et al. Acebutolol in supraventricular arrhythmias. Clin
Pharmacol Ther 1979; 25:149.
36. Williams DO, Tatelbaum R, Most AS. Effective treatment of supraventricular arrhythmias with
acebutolol. Am J Cardiol 1979; 44:521.
37. Pierce WJ, McGroary K. Multifocal atrial tachycardia and Ibutilide. Am J Geriatr Cardiol 2001;
10:193.
38. Kones RJ, Phillips JH, Hersh J. Mechanism and management of chaotic atrial mechanism.
Cardiology 1974; 59:92.
39. Ueng KC, Lee SH, Wu DJ, et al. Radiofrequency catheter modification of atrioventricular junction
in patients with COPD and medically refractory multifocal atrial tachycardia. Chest 2000; 117:52.

Topic 901 Version 14.0

GRAPHICS

Relationship between myocardial action potential and

surface electrocardiogram

Each phase of the myocardial action potential (numbers, upper panel)

corresponds to a deflection or interval on the surface electrocardiogram
(lower panel). Phase 4, the resting membrane potential, is responsible for
the TQ segment; this segment has a prominent role in the ECG
manifestations of ischemia during exercise testing.

Graphic 64133 Version 2.0

Electrocardiogram (ECG) showing multifocal atrial tachycardia

Electrocardiogram (ECG) showing multifocal atrial tachycardia in a patient with severe

pulmonary disease. The diagnostic criteria include an average atrial rate above 100
beats/min and at least three different non-sinus P waves in the same lead. Note the
multiple P wave morphologies - inverted (I), upright (U), and biphasic (B).

Courtesy of Ary Goldberger, MD.

Graphic 70173 Version 4.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS
duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

Pharmacologic agents for acute heart rate control in patients with
multifocal atrial tachycardia and chronic obstructive pulmonary disease

Initial Subsequent Maintenance

Drug Onset Side effects
dose doses dose

Verapamil* ¶ ◊ 1 mg IV 1 to 2 4 mg over 5 120 to 480 mg Hypotension, heart

minutes minutes; then daily block, heart failure
5 mg over 5
minutes up to 3
additional
doses

Metoprolol Δ ¶ ◊ 5 mg IV 5 minutes 5 mg IV over 5 50 to 100 mg Hypotension, heart

over 5 minutes at 10 orally twice daily block, bradycardia,
minutes minute heart failure,
intervals for 2 bronchoconstriction
to 3 additional
doses

MAT: multifocal atrial tachycardia; COPD: chronic obstructive pulmonary disease.

* For all patients with COPD and MAT and a rapid ventricular response, correction of hypoxemia, acidosis,
and other metabolic disturbances is recommended. Theophylline can increase the ventricular response, so
dosing should be regulated to keep the serum level in the range of 8 to 12 mg/mL; discontinuation of the
medication should be considered.
¶ Verapamil is preferred over metoprolol for heart rate control of MAT in patients with COPD due to concerns
about exacerbating bronchoconstriction.
Δ Representative of the type of selective beta-1 blockers that could be used, but similar drugs could be
given in appropriate doses.
◊ Verapamil and beta blockers should not be given to patients with sinus node dysfunction or preexisting
second- or third-degree block unless a temporary or permanent pacemaker has been implanted. Verapamil
and beta blockers should be administered cautiously in patients with decompensated heart failure or
hypotension to avoid worsening these conditions.

Graphic 83358 Version 5.0

Contributor Disclosures
Alfred Buxton, MD Grant/Research/Clinical Trial Support: Medtronic [Left ventricular activation
(CRT devices)]; Biosense-Webster [Left ventricular activation in LBBB (CRT devices)]. Leonard I
Ganz, MD, FHRS, FACC Speaker’s Bureau: Amgen [Heart failure (Ivabradine)]; Pfizer, BMS
[Anticoagulation (Apixaban)]; St. Jude Medical, Biotronik [Cardiac rhythm (Pacemaker/ICD)];
Lundbeck [Orthostatic hypotension (Northera)]. Consultant/Advisory Boards: Unequal Technologies
[Commotio cordis (Protective equipment)]. Equity Ownership/Stock Options: Unequal Technologies
[Commotio cordis (Protective equipment/apparel)]. Brian C Downey, MD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy