Dr Mohamed Salih Aziz
King Abdualaziz Medical City Riyadh
Atrial tachycardia is defined as a
supraventricular tachycardia (SVT) that
does not require the atrioventricular (AV)
junction, accessory pathways, or
ventricular tissue for initiation and
maintenance of the tachycardia
The ECG typically shows a narrow QRS complex
tachycardia (unless bundle branch block aberration
Heart rates during atrial tachycardia are highly variable,
with a range of 100-250 beats per minute
The atrial rhythm is usually regular
The conducted ventricular rhythm is also usually
regular but may become irregular, often at higher atrial
rates because of variable conduction through the AV
node, thus producing conduction patterns such as 2:1,
3:1, and Wenckebach AV block.
The P wave morphology may give clues to the site
of origin and mechanism of the atrial tachycardia.
In the case of a focal tachycardia, the P wave
morphology and axis depend on the location in the
atrium from which the tachycardia originates. In the
case of macroreentrant circuits, the P wave
morphology and axis depend on activation patterns.
Types of Atrial Tachycardia
A-Based on endocardial activation:
2) focal atrial tachycardia
arises from a localized area in the atria such as
the crista terminalis, pulmonary veins, ostium of
the coronary sinus, or atrial septum. Focal atrial
tachycardia that originates from the pulmonary
veins may trigger atrial fibrillation
2) reentrant atrial tachycardias .
most commonly occur in persons with structural
heart disease, complex heart disease, and
particularly after surgery involving incisions or
scarring in the atria. these atrial tachycardias are
similar to the typical atrial flutters
3)Sinoatrial reentrant tachycardia
is a subset of focal atrial tachycardia due to reentry
arising within the sinus node situated at the
superior aspect of the crista terminalis. The P wave
morphology and atrial activation sequence are
similar to those of sinus tachycardia
is a unique type of atrial tachycardia in which atrial
activation originates from multiple atrial foci.
MAT often occurs in patients experiencing an
exacerbation of chronic obstructive pulmonary
disease, a pulmonary thromboembolism, an
exacerbation of congestive heart failure, or
severe illness especially under critical care with
It is often associated with hypoxia and
Digitalis toxicity also may be present in persons
with MAT, with triggered activity as the
Pat hophysi ol ogi c mechani sms
Several pathophysiologic mechanisms have been
ascribed to atrial tachycardia. These mechanisms can be
differentiated based on the pattern of onset and
termination and response to drugs and atrial pacing.
Automatic atrial tachycardia
is observed both in patients with normal heart structure
and in those with organic heart disease.
The tachycardia typically exhibits a warm-up
phenomenon, during which the atrial rate gradually
accelerates after its initiation and slows prior to its
It is rarely initiated or terminated by single atrial
stimulation or rapid atrial pacing, but it may be transiently
suppressed by overdrive pacing.
Carotid sinus massage and adenosine do not terminate
the tachycardia even if they produce a transient AV
Electrical cardioversion is ineffective (being equivalent to
attempting electrical cardioversion in a sinus tachycardia
is due to delayed after-depolarizations
occurs in patients with digitalis intoxication or conditions
associated with excess catecholamines.
the arrhythmia can be initiated, accelerated, and terminated by
rapid atrial pacing.
It may be sensitive to physiologic and pharmacologic
maneuvers such as adenosine, verapamil, and beta-blockers,
which all can terminate the tachycardia. Occasionally, this atrial
tachycardia may arise from multiple different sites in the atria,
producing a multifocal or multiform atrial tachycardia. This may
be recognized by varying P wave morphology and irregularity in
the atrial rhythm.
Intra-atrial reentry tachycardias may have either a
macroreentrant or a microreentrant circuit.
Macroreentry is the usual mechanism in atrial flutter and in
scar- and incision-related (postsurgical) atrial tachycardia.
Microreentry can arise in a small focal area such as in sinus
node reentrant tachycardia.
Typically, reentrant atrial tachycardia arises suddenly,
terminates suddenly, and is paroxysmal.
Carotid sinus massage and adenosine are ineffective in
terminating the tachycardia even if they produce a transient AV
nodal block. On electrophysiologic study,
it can be induced and terminated by programmed
extrastimulation. As is typical in other reentry tachycardias,
electrical cardioversion terminates this type of atrial
Typically, atrial tachycardia manifests as a sudden
onset of palpitations.
If atrial tachycardia is due to enhanced automaticity,
it may be nonsustained but repetitive or continuous
or sustained, as in reentrant forms of atrial
Patients may present with a tachycardia that
gradually speeds up soon after its onset (warm-up
phenomenon). The patient may be unaware of this.
This finding during ECG monitoring, as with a Holter,
is suggestive that the supraventricular tachycardia is
•If accompanied by palpitations, patients also may report
dyspnea, dizziness, lightheadedness, fatigue, or chest
pressure. One should recognize the early manifestations of
tachycardia-induced cardiomyopathy, ie, a decline in effort
tolerance and symptoms of heart failure, in patients with
frequent or incessant tachycardias.
* Lightheadedness may result from relative hypotension,
depending on the heart rate and other factors such as the
state of hydration and particularly the presence of structural
heart disease. The faster the heart rate, the more likely a
patient is to feel lightheaded. If the patient has a rapid rate
and severe hypotension, syncope may occur.
The primary abnormality noted upon physical
examination is a rapid pulse rate. In most atrial
tachycardias this is regular. However, in rapid atrial
tachycardias with variable AV conduction and in
multifocal atrial tachycardia (MAT), the pulse may be
Blood pressure may be low in those patients with
fatigue, lightheadedness, or presyncope.
The cardiovascular examination should be aimed at
excluding underlying structural heart diseases such as
valvular abnormalities and evidence of heart failure.
Abnormal thyroid function should also be in the
Atrial Tachycardia With 3:2 and 2:1 AV Block-KH
The ectopic atrial rate is 150 bpm. Some of the
ectopic P waves are easily seen and indicated
by the arrows. Other P waves are burried in the
T waves and not so easily identified. Atrial
tachycardia with AV block is often a sign of
digitalis intoxication. 3:2 and 2:1 AV block is
seen in this example.
The ectopic P waves, easily seen in this example,
occur in groups, separated by short pauses. This
is likely due to an exit block just distal to the atrial
pacemaker. Because not all of the P waves make
it to the ventricles, there is also 2nd degree AV
block. Therefore, two levels of block are present:
one in the atria and one at the level of the AV
Very Subtle Atrial Tachycardia With 2:1 Block-KH
Frank Yanowitz Copyright 1996
Although at first glance this looks like normal sinus
rhythm at 95 bpm. On closer look, there are 2 'P'
waves for every QRS; the atrial rate is 190 bpm.
Note the hidden 'P' in the T waves. This rhythm is
likely due to digitalis intoxication, as are the GI