What is atrial tachycardia

Atrial tachycardia usually occurs for brief periods and starts and stops spontaneously. That's called paroxysmal AT. If it continues, it is called persistent AT. Atrial tachycardia occurs most commonly in elderly patients and those with other types of heart disease, though it occasionally appears in children, younger people and those with healthy hearts.

Causes include:. But when atrial tachycardia is an occasional event, an office ECG may be normal. If this is the case, your doctor may give you an ECG monitor to wear at home that will record your heart rhythm over time.

These include:. However, treatment decisions are based on a more fine-tuned study of where and how the electrical signals are produced. Your doctor may recommend an electrophysiological study of your heart, during which a narrow, flexible tube called a catheter is threaded through a vein to your heart under light sedation. Fine wires inside the catheter can help pinpoint the origin of the errant electrical signal. Color coding corresponds to activation timing.

Areas red-yellow correspond to early activation and blue-purple late activation. The anatomic location where early meets late corresponds to the isthmus of the tachycardia. LAA: left atrial appendage. Short, self-terminated runs of atrial tachycardia are rather common in ambulatory heart rhythm monitor recordings; but when asymptomatic and sporadic, they are frequently dismissed as incidental findings and not considered a clinical entity.

Atrial tachycardias become more prevalent with age at the expense of a higher representation of macro-reentrant atrial tachycardias in the older population, while focal atrial tachycardias become rather rare. Focal atrial tachycardias are more common among younger patients with normal hearts. A gender difference in the prevalence of these arrhythmias is not clear, although higher prevalence of focal automatic atrial tachycardias in women has been reported.

The other forms of supraventricular tachycardia are very difficult to differentiate from atrial tachycardias from the clinical standpoint:.

Atypical AV nodal reentrant tachycardia fast-slow or slow-slow AVNRT : electrocardiographically very difficult to differentiate from an atrial tachycardia. An electrophysiology study may be necessary to make a definitive diagnosis. Atrioventricular reentrant tachycardia AVRT : during tachycardia, the P waves are usually close to the preceding QRS in AVRT resulting in a rather long P—R interval, which suggests a diagnosis different than atrial tachycardia but still possible in atrial tachycardias with prolonged P—R.

Permanent junctional reciprocating tachycardia a unique form of AV reentrant tachycardia using a slow conducting retrograde accessory pathway : because of the participation of a slowly conducting accessory pathway as the retrograde limb of the tachycardia, this arrhythmia has retrograde P waves with a superior axis close to the following QRS resulting in a relatively normal P—R interval and very difficult to differentiate from an atrial tachycardia.

The incessant nature of this arrhythmia, younger age of presentation, and frequent presentation as tachycardia-induced cardiomyopathy help lead the clinical differential diagnosis towards this entity.

Junctional ectopic tachycardia: rather rare and more common in children. As a focal tachycardia originating in AV nodal tissue, it clinically presents similar to focal atrial tachycardias, but the electrocardiographic recordings are similar to those of typical AV nodal reentrant tachycardia usually showing absence of P waves that are simultaneous and obscured by the QRS. An electrophysiology study with pacing maneuvers is necessary to make a definitive diagnosis.

Ventricular tachycardia: any supraventricular tachycardia that conducts to the ventricle with aberrancy resulting in a wide complex tachycardia, either due to bundle branch block or intraventricular conduction delay underlying at baseline or developed during tachycardia , could resemble ventricular tachycardia. The clinical setting, characteristics of the arrhythmia, and AV relationship are useful in establishing the diagnosis, although not infrequently an electrophysiology study with intracardiac recordings is needed.

In the differential diagnosis of supraventricular tachycardias, the administration of an intravenous bolus of adenosine 6, 12, or 18 mg administered rapidly and followed by a large bolus of saline flush may be helpful. If intravenous adenosine does not terminate the tachycardia and results in AV block with continuation of the tachycardia in the atrium, the diagnosis of atrial tachycardia is confirmed.

If the tachycardia terminates with intravenous adenosine, the mechanism of the tachycardia may be suspected as reentrant and possibly with the participation of the AV node but no definitive conclusion can be drawn since some focal atrial tachycardias, as well as macroreentrant atrial tachycardias, could terminate with intravenous adenosine. Atrial flutter: the characteristic electrocardiographic pattern and atrial rate around bpm establishes the differential diagnosis.

Nevertheless, in practice, there is an overlap between macroreentrant atrial tachycardias and atrial flutter. By mechanism, typical atrial flutter a circuit of reentry in the right atrium using the cavo-tricuspid isthmus as the critical isthmus is a form of macro-reentrant atrial tachycardia and many macro-reentrant atrial tachycardias could be considered forms of atypical atrial flutter, and manifest clinically and in the electrocardiogram as atrial flutter.

A definitive diagnosis can only be made in the electrophysiology laboratory with the characterization of the tachycardia circuit. Atrial fibrillation: the characteristic electrocardiographic pattern of fibrillatory waves in the electrocardiogram and irregularity of the arrhythmia are diagnostic of atrial fibrillation.

Inappropriate sinus tachycardia: often difficult to differentiate from an atrial tachycardia. Symptoms, clinical presentation, and patient population are very similar. The electrocardiogram during tachycardia shows P waves identical to the P waves during slower rates.

Overlap of the P wave with the preceding T wave may make the comparison of the P waves difficult. An ambulatory heart rhythm monitor to document the progressive acceleration and deceleration of inappropriate sinus tachycardia without a sudden onset or change in P wave morphology is often required.

The characteristic development of tachycardia and symptoms with upright posture and resolution of the symptoms help differentiate this syndrome from the other forms of supraventricular tachycardias. Physiologic sinus tachycardia: the P waves during tachycardia are identical to the P waves at slower rates. An underlying cause for the tachycardia eventually becomes apparent including anemia, volume depletion, hypoxia, pain, anxiety, or a drug effect i.

The landmark physical finding in atrial tachycardias is the tachycardia itself, with a heart rate above bpm and rarely dropping below but faster than the underlying sinus rhythm. Frequently, patients have no other physical findings related to the arrhythmia and while not in tachycardia their physical exam may be completely normal.

Depending on the physiologic effects and rate of the tachycardia, like with any other supraventricular tachycardia, the patient may present the following symptoms during the arrhythmia:. Underlying conditions that could predispose the development of atrial tachycardias may have more specific physical findings.

Heart murmur in the case of valvular heart disease, hypertrophic cardiomyopathy, and congenital heart disease; sustained apical impulse in the case of left ventricular hypertrophy, barrel chest, tachypnea, or adventitious lung sounds in patients with underlying pulmonary disease.

The physical examination does not provide specific findings confirmatory of the diagnosis of atrial tachycardia. Vagal maneuvers like Valsalva, carotid sinus massage limited to patients without suspected carotid occlusive disease , and cold drinks, among others, may terminate the tachycardia and suggest the diagnosis of a supraventricular tachycardia but have no value on the specific diagnosis of an atrial tachycardia.

Laboratory studies may be helpful in the diagnosis of underlying or associated conditions as well as in the differential diagnosis of sinus tachycardia but no laboratory test is useful in the specific diagnosis of an atrial tachycardia.

As an example, a complete blood count aids in the diagnosis of anemia or potential underlying infections; thyroid function tests help to address the clinical suspicion of thyroid disease; a blood gas analysis determines the presence and severity of hypoxia in predisposing pulmonary conditions; serum level of brain natriuretic peptide complements the evaluation of associated heart failure; and renal function tests and creatinine clearance have implications on the choice of antiarrhythmic drug.

The diagnosis of supraventricular tachycardias and specifically atrial tachycardias is established with the documentation and characterization of the heart rhythm as discussed in section II E 2 below. Documentation of the tachycardia and evaluation of the underlying cardiac condition are fundamental in the diagnosis and management of this arrhythmia:. ECG: a lead electrocardiogram recorded in sinus rhythm and during tachycardia. P waves during tachycardia exhibiting an axis different than expected for sinus tachycardia and a normal or short P—R interval is compatible with the diagnosis of atrial tachycardia.

A similar electrocardiogram can be seen with the so-called atypical fast-slow or slow-slow variants of AV nodal reentrant tachycardia and in persistent junctional reciprocating tachycardia atrioventricular reentrant tachycardia using a slow conducting retrograde accessory pathway. A long P—R interval during tachycardia does not exclude an atrial tachycardia since atrial tachycardias conducted either over the slow pathway of the AV node, a diseased AV node, or an AV node slowed by drugs or increased vagal tone could result in a prolonged P—R interval during the arrhythmia.

Paroxysmal atrial tachycardias are frequently elusive and difficult to document in a lead electrocardiogram Figure 1, Figure 3. Ambulatory heart rhythm monitors include the traditional Holter monitor usually limited to 24 to 48 hours of heart rhythm recording , portable continuous tele-monitors with ongoing heart rhythm transmission and recording, snapshot event recorders and event loop recorders, which could be portable or implantable. These monitors could be single or multichannel and the recording of a sudden onset and offset of tachycardia with P wave morphology different than the one in sinus rhythm is suggestive of the diagnosis of supraventricular tachycardia.

Electrophysiology study: the definitive diagnosis confirmation of an atrial tachycardia is best done in the electrophysiology laboratory. Intracardiac recordings and response to pacing maneuvers during tachycardia, as well as characteristics of tachycardia induction and activation maps, provide a definitive diagnosis of the mechanism of the tachycardia as well as an opportunity for definitive treatment through ablation.

Advanced nonfluoroscopic three-dimensional mapping systems with computerized representation of the cardiac chambers where activation and signal characteristics can be displayed are available today to facilitate the diagnosis and therapy in the electrophysiology laboratory Figure 2, Figure 4.

Echocardiogram: indicated for the evaluation of potential or known underlying structural heart disease. The treatment of atrial tachycardias is focused on rhythm control and prevention of arrhythmia recurrence. Persistent tachycardias with hemodynamic compromise must be terminated emergently with electrical cardioversion.

In the case of persistent focal atrial tachycardias and frequently in the management of macro-reentrant atrial tachycardias that resemble atrial flutter, the initial treatment may be aimed at rate control but more definitive treatment and resolution of the clinical symptoms usually requires restoration of normal sinus rhythm.

The treatment could be pharmacologic or catheter based ablation. The patient should participate in the decision of which strategy to use as long as he or she can be a candidate for both. Patients with multiple comorbidities and contraindications for antiarrhythmic drugs should be treated with an invasive strategy, and patients with vascular access problems, contraindication to sedatives, and inability to safely withstand an ablation procedure should be treated with a conservative approach until they can be candidates for an invasive procedure.

Pharmacologic therapy includes beta-blockers, calcium channel blockers, and antiarrhythmic drugs. Among antiarrhythmic drugs, class IC seem to be particularly effective with focal atrial tachycardias, but its use is limited to patients without myocardial scar and by extension, patients without coronary artery disease or significant structural heart disease. Sotalol, amiodarone, and dofetilide can be used as well. Dofetilide have been reported to be more effective in the management of atrial flutter and hence suspected to be more effective for macro-reentrant atrial tachycardias but limited by the QTc and creatinine clearance.

Treatment through catheter based ablation is the preferred approach given its high success rate and potential freedom of arrhythmias without the need for continued drug therapy. The catheter ablation procedure is a percutaneous invasive intervention that requires vascular access through the femoral and sometimes subclavian veins. Catheters with electrodes are advanced into the heart under fluoroscopy and used for recording intracardiac signals and stimulating the heart.

With the use of pacing maneuvers and pharmacologic interventions, the tachycardia can be induced if not present at the time of the procedure and characterized establishing a definitive diagnosis of atrial tachycardia and differentiating between focal and macro-reentrant.

Radiofrequency energy or cryoablation are delivered through a catheter tip to eliminate the tissue where a focal atrial tachycardia originates or tissue that is critical for the reentry circuit Figure 4, Figure 5.

Surface and intracardiac electrogram recordings during ablation and termination of the macro-reentrant atrial tachycardia shown in Figures 3 and 4. The asterisks mark the double potentials corresponding to the area of slow conduction functioning as isthmus of the reentrant tachycardia.

Once radiofrequency ablation eliminates conduction in the isthmus, only one component of the double potential is recorded at the time of tachycardia termination. Conduction block is created in the area of slow conduction, rendering the tachycardia not inducible.

The procedure may require access to the left atrium performing a transseptal puncture or retrograde through the aorta. The contemporary approach to catheter-based ablation using nonfluoroscopic mapping systems, intracardiac echocardiography, and irrigated tip catheters allows for improved safety during the procedure.

Macro-reentrant atrial tachycardias associated to extensive atrial fibrosis in patients with valvular heart disease, multiple extensive atrial ablations, or surgeries may be particularly difficult to control both with drugs or ablation and eventually may require an aggressive rate-control strategy with AV junction ablation and the implantation of a permanent pacemaker. During tachycardia in the acute setting hemodynamic support and restoration of adequate perfusion should remain the priority as mandated by the ACLS protocols.

When there is evidence of hemodynamic compromise restoration of normal sinus rhythm and perfusion should be achieved immediately through CPR, electrical cardioversion, and vasoactive drugs.

Intravenous hydration is recommended during tachycardia in the absence of signs and symptoms of congestive heart failure. If the blood pressure is not critically compromised, a bolus of intravenous adenosine can help in establishing the diagnosis or terminating the tachycardia. Vagal maneuvers including carotid sinus massage are also helpful either in terminating a supraventricular tachycardia or causing transient AV nodal block to allow the diagnosis of an atrial tachycardia when the atrial tachycardia continues despite conduction block to the ventricle.

Antiarrhythmic drugs in the acute setting can also be used for pharmacologic conversion of an incessant tachycardia or to achieve rate control and symptomatic relief.

Beta-blockers are the first-line of therapy, particularly if there blood pressure is stable. Other antiarrhythmic drugs include class Ic antiarrhythmics given orally flecainide to mg, propafenone mg , intravenous amiodarone and ibutilide.

Intravenous calcium channel blockers or digoxin can be attempted for rate control, especially in faster tachycardias macro-reentrant atrial tachycardias that resemble atrial flutter in which AV nodal blocking agents could be expected to slow ventricular response.

Procainamide, disopyramide, and quinidine are rarely used. Class Ic antiarrhythmic drugs flecainide, propafenone, procainamide, and disopyramide should be only given to patients with macro-reentrant atrial tachycardias and atrial flutter when administered together with AV nodal blocking agents to prevent slowing of the tachycardia cycle length and AV conduction that could lead to hemodynamic instability.

Blood pressure and pulse rate should be monitored during the treatment of the arrhythmia in the acute setting, although a heart rhythm monitor or electrocardiogram is of most value. When the tachycardia is accompanied by signs of heart failure, dizziness, or syncope, monitoring respiratory rate, pulse oximetry, body weight, lung sounds, jugular venous distention, peripheral edema, urinary output, and neurologic and mental status is warranted to prevent worsening of those conditions that may be a consequence of coexisting with the tachycardia.

Continuous heart rhythm monitoring and lead electrocardiograms to document and analyze rhythm changes is of most value to monitor the response to therapy. Laboratory tests are usually not needed unless used to guide response to concomitant therapy for other associated conditions or complications of the arrhythmia:. This causes the atrial chambers of the heart to quiver instead of pump.

When this happens only part of the blood is forced out of the heart chamber. The blood pools inside the atrium and sometimes clots. These blood clots can cause a stroke if they break off and block an artery in the brain.

Although atrial fibrillation isn't life threatening, it can lead to other rhythm problems, chronic fatigue and congestive heart failure. Some people with atrial fibrillation do not feel anything different. Others notice an abnormal feeling right away. If you have atrial fibrillation, you may feel a racing, uncomfortable, irregular heartbeat and a 'flopping' in your chest.

Dizziness, sweating, and chest pain or pressure can also occur. Other symptoms include shortness of breath, overall weakness, and the inability to exercise. Certain risk factors make it more likely to develop atrial fibrillation, but often the cause remains unclear.

Leading risk factors include:. Gender and age also affect both the likelihood of developing atrial fibrillation and the severity of the condition. Men are slightly more likely than women to have atrial fibrillation, but women who are diagnosed with the disease have a greater risk over time for premature death. Older people are more likely to have atrial fibrillation than younger people.

Additional risk factors include thyroid disorders, diabetes, high blood pressure, excessive alcohol intake, and cigarette or drug use including caffeine. Arrythmias that begin above the ventricles are called supraventricular tachycardia SVT. In this condition a series of early beats in the atria speeds up the heart rate. There are two main types of supraventricular tachycardia:. Sinus tachycardia is a normal increase in the heart rate.

It is caused when the sinus node sends out signals faster than usual.