History
Focal atrial tachycardia is usually episodic or paroxysmal. Typically, atrial tachycardia manifests as a sudden onset of palpitations. Atrial tachycardia due to enhanced automaticity may be nonsustained but repetitive or it may be continuous or sustained, as in reentrant forms of atrial tachycardia.
Atrial tachycardia may gradually speed up soon after its onset ("warm-up" phenomenon) and gradually slows down before termination ("cool-off" phenomenon). However, the patient may be unaware of this. In a patient with supraventricular tachycardia (SVT), the presence of warm-up phenomenon on an electrocardiogram (eg, on Holter monitoring) suggests that the SVT is atrial tachycardia.
If the tachycardic episodes are accompanied by palpitations, patients also may report dyspnea, dizziness, lightheadedness, fatigue, or chest pressure. In patients with frequent or incessant tachycardias, a decline in effort tolerance and symptoms of heart failure may represent early manifestations of tachycardia-induced cardiomyopathy.
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. A rapid rate and severe hypotension may lead to syncope.
Reentrant atrial tachycardia is not uncommon in patients with a history of a surgically repaired atrial septal defect. The scar tissue in the atrium may give rise to the formation of a reentrant circuit.
The history should include questions regarding possible causes, such as the following:
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Medical history, especially history of tachycardia or other cardiac problems
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Medications: Amphetamines, cocaine, caffeine, ephedrine, antihistamines, phenothiazines, antidepressants, theophylline, appetite suppressants, albuterol, digoxin
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Family history of sudden death, deafness (Jervell-Lange Nielsen syndrome), or cardiac disease
Underlying disorders in multifocal atrial tachycardia
In patients with multifocal atrial tachycardia (MAT), the history may disclose an underlying illness that is causing the tachycardia. Such illnesses include pulmonary, cardiac, metabolic, and endocrinopathic disorders.
Chronic obstructive pulmonary disease (COPD) is the most common underlying disease process (60%). The arrhythmia is commonly precipitated by exacerbation of COPD, sometimes due to infection or exacerbation of heart failure. Increasing hypoxemia with respiratory acidosis and advanced disease also leads to increased bronchodilator usage, thereby increasing catecholamine levels, which may contribute to development of MAT.
Patients with MAT frequently have structural heart disease, mainly coronary artery disease and valvular heart disease, often in conjunction with COPD. Heart failure is often present when the diagnosis of MAT is first made. Metabolic disorders may also lead to MAT. In various series, 24% of patients with MAT were found to have diabetes mellitus, 14% had hypokalemia, and 14% had azotemia.
Twenty-eight percent of patients with MAT are recovering from major surgery, while others have postoperative infections, sepsis, pulmonary embolism, and heart failure. The link between pulmonary embolism and MAT is weak (ie, 6-14% of such patients have been said to have MAT), but the methods of diagnosing pulmonary embolism in these cases have not been well documented.
Physical Examination
The primary abnormality noted on physical examination is a rapid pulse rate. In most atrial tachycardias, the rate is regular. However, in rapid atrial tachycardias with variable atrioventricular (AV) conduction and in MAT, the pulse may be irregular.
Blood pressure may be low in patients presenting with fatigue, lightheadedness, or presyncope. The cardiovascular examination should be aimed at excluding underlying structural heart diseases such as valvular abnormalities and heart failure.
Depending upon comorbid conditions or general health status, the patient may be hemodynamically unstable. However, determining whether this is due to the underlying condition or to the arrhythmia may be difficult.
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Atrial tachycardia. This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note that the negative P waves in leads III and aVF (upright arrows) are different from the sinus beats (downward arrows). The RP interval exceeds the PR interval during the tachycardia. Note also that the tachycardia persists despite the atrioventricular block.
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Atrial tachycardia. This propagation map of a right atrial tachycardia originating from the right atrial appendage was obtained with non-contact mapping using the EnSite mapping system.
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Atrial tachycardia. Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features essentially exclude atrioventricular nodal reentry tachycardia and atrioventricular tachycardia via an accessory pathway. Note also that the change in the P-wave axis at the onset of tachycardia makes sinus tachycardia unlikely.
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Atrial tachycardia. An anterior-posterior mapping projection is shown. This is an example of activation mapping using contact technique and the EnSite system. The atrial anatomy is partially reconstructed. Early activation points are marked with white/red color. The activation waveform spreads from the inferior/lateral aspect of the atrium through the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. CS = shadow of the catheter inserted in the coronary sinus; TV = tricuspid valve.
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Atrial tachycardia. These intracardiac tracings showing atrial tachycardia breaking with the application of radiofrequency energy. Before ablation, the local electrograms from the treatment site preceded the surface P wave by 51 ms, consistent with this site being the source of the tachycardia. Note that postablation electrograms on the ablation catheter are inscribed well past the onset of the sinus rhythm P wave. The first three tracings show surface electrocardiograms as labeled. Abl = ablation catheter (D-distal pair of electrodes); CS = respective pair of electrodes of the coronary sinus catheter; CS 1,2 = distal pair of electrodes; CS 7,8 = electrodes located at the os of the coronary sinus.
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Atrial tachycardia. This image shows an example of rapid atrial tachycardia mimicking atrial flutter. A single radiofrequency application terminates the tachycardia. The first three tracings show surface electrocardiograms, as labeled. AblD and AblP = distal and proximal pair of electrodes of the mapping catheter, respectively; HBED and HBEP = distal and proximal pair of electrodes in the catheter located at His bundle, respectively; HRA = high right atrial catheter; MAP = unipolar electrograms from the tip of the mapping catheter; RVA = catheter located in right ventricular apex.
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Atrial tachycardia. This electrocardiogram shows multifocal atrial tachycardia (MAT).
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Atrial tachycardia. This electrocardiogram belongs to an asymptomatic 17-year-old male who was incidentally discovered to have Wolff-Parkinson-White (WPW) pattern. It shows sinus rhythm with evident preexcitation. To locate the accessory pathway (AP), the initial 40 milliseconds of the QRS (delta wave) are evaluated. Note that the delta wave is positive in lead I and aVL, negative in III and aVF, isoelectric in V1, and positive in the rest of the precordial leads. Therefore, this is likely a posteroseptal AP.
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Atrial tachycardia. This is a 12-lead electrocardiogram from an asymptomatic 7-year-old boy with Wolff-Parkinson-White (WPW) pattern. Delta waves are positive in leads I and aVL; negative in II, III, and aVF; isoelectric in V1; and positive in the rest of the precordial leads. This again predicts a posteroseptal location for the accessory pathway (AP).
Tables
Type of Tachycardia |
Treatment (Grade) |
Not Mentioned in 2019 Guidelines |
Narrow QRS tachycardias |
Verapamil and diltiazem; beta-blockers (now all are grade IIa) |
Amiodarone, digoxin |
Wide QRS tachycardias |
Procainamide, adenosine (both grade IIa); amiodarone (IIb) |
Sotalol, lidocaine |
Inappropriate sinus tachycardia |
Beta-blockers (IIa) |
Verapamil/diltiazem, catheter ablation |
Postural orthostatic tachycardia syndrome |
Salt and fluid intake (IIb) |
Head-up tilt sleep, compression stockings, selective beta-blockers, fludrocortisone, clonidine, methylphenidate, fluoxetine, erythropoietin, ergotaminel octreotide, phenobarbitone |
Focal atrial tachycardia |
Acute: beta-blockers (IIa); flecainide/propafenone, amiodarone (IIb) |
Acute: procainamide, sotalol, digoxin |
Chronic: beta-blockers; verapamil and diltiazem (all IIa) |
Chronic: amiodarone, sotalol, disopyramide |
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Atrial flutter |
Acute: ibutilide (I); verapamil and diltiazem, beta-blockers (all IIa); atrial or transesophageal pacing (IIb); flecainide/propafenone (III) |
Acute: digitalis |
Chronic: — |
Chronic: dofetilide, sotalol, flecainide, propafenone, procainamide, quinidine, disopyramide |
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Atrioventricular nodal re-entrant tachycardia (AVNRT) |
Acute: — |
Acute: amiodarone, sotalol, flecainide, propafenone |
Chronic: verapamil and diltiazem; beta-blockers (all IIa) |
Chronic: amiodarone, sotalol, flecainide, propafenone, “pill-in-the-pocket” approach |
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Atrioventricular re-entrant tachycardia (AVRT) |
Beta-blockers (IIa); flecainide/propafenone (IIb) |
Amiodarone, sotalol, “pill-in-the-pocket” approach |
SVT in pregnancy |
Verapamil (IIa); catheter ablation (IIa when fluoroless ablation is available) |
Sotalol, propafenone, quinidine, procainamide |
Adapted from Brugada J, Katritsis DG, Arbelo E, et al, for the ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2019 Aug 31;ehz467. https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz467/5556821 |
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