Sinoatrial nodal reentry tachycardia is an uncommon form of sinus tachycardia. The clinical presentation is similar to that of other regular narrow-complex tachycardias. The condition is not as benign as previously thought and is associated with organic heart disease. The challenges in the management of this complex tachycardia are to make an appropriate and timely diagnosis and to provide proper treatment based upon the patient's clinical condition. Several clinical and electrocardiographic clues, such as the onset of the arrhythmia and the P-wave characteristics, can be obtained at the bedside and help distinguish this arrhythmia from other types. Current treatment recommendations include the use of antiarrhythmic agents and, in some cases, electrophysiologic ablation.

Sinoatrial nodal reentry tachycardia, also known as sinus reentry tachycardia, was initially described in 1943. Narrow-complex tachycardias, also known as supraventricular tachycardias, are frequently seen in hospitalized patients and are a common reason for emergency department visits.¹ In the general population, the incidence of supraventricular tachycardias (excluding atrial fibrillation and flutter) is 35 per 100,000.² It is imperative to diagnose appropriately the etiology of the tachycardia, because management differs, and what is therapeutic for one arrhythmia is potentially deleterious for others. For example, although many of the reentry arrhythmias respond well to beta-receptor antagonists, it is hazardous to treat an appropriate sinus tachycardia—secondary to an infection or status asthmaticus—with this agent, because it may further compromise the patient's hemodynamic status.

Etiology

Sinus tachycardias account for the majority of arrhythmias. The etiology can be physiologic, such as physical exertion or anxiety; pathologic, such as blood loss or thyrotoxicosis; or pharmacologic, which is induced by a prescribed drug (eg, dobutamine) or an illicit substance (eg, cocaine).

Most sinus tachycardias share the common stimulating pathway of increased sympathetic stimulation of the sinus node. Other mechanisms that have been implicated in sinus tachycardias include hypoxia, methylxanthine stimulation (from coffee or tea intake), and increased serotonin levels (from antidepressant therapy or the use of illicit drugs, such as lysergic acid diethylamide [LSD]). The other causes of sinus tachycardias are much less common than appropriate sinus tachycardia and are often overlooked.

Inappropriate sinus tachycardia was first recognized in a family cluster in 1941. About 90% of patients with this condition are female, and healthcare workers seem to be disproportionately affected (plausibly because of greater self-assessment in this population).3

Two causes have been proposed for the pathologic basis of inappropriate sinus tachycardia (although the exact mechanism has yet to be discerned)3: (1) An imbalance in the autonomic innervation of the sinus node favoring sympathetic input, and (2) enhanced automaticity of the sinus node.

Postural orthostatic tachycardia syndrome is another type of sinus tachyarrhythmia related to autonomic dysfunction that is clinically manifested by excessive orthostatic tachycardia, without significant orthostatic hypotension.³

Sinoatrial nodal reentry tachycardia has been found in both human and animal hearts. A reentry circuit in or around the sinus node is probably responsible, although the exact location of the reentry circuit has yet to be established.⁴

Illustrative Case

An 82-year-old white man was transferred from a nursing facility to the emergency department after a house nurse noticed that his pulse was rapid and irregular. The patient was asymptomatic but had a history of paroxysmal atrial fibrillation and coronary artery disease and had coronary artery bypass surgery several years ago.

On initial evaluation, vital signs were within normal limits. Physical examination revealed a well-nourished, overweight man in no distress. Cardiac examination demonstrated a regular rhythm, without murmurs or gallops. The lungs were clear to auscultation, and the rest of the examination was within normal limits.

An electrocardiogram (ECG) was obtained, showing normal sinus rhythm, with a right bundle-branch block that had been noted on previous ECGs. The patient was then evaluated in a telemetry setting for 24 hours. The patient's heart rate was noted on the telemetry monitor to have suddenly increased to 190 beats/min; further evaluation showed he was asymptomatic: blood pressure, 130/78 mm Hg; a confirmed pulse in the 190s.

A 12-lead ECG was obtained (Figure 1), and the patient was treated with 6 mg of intravenous (IV) adenosine (Adenocard), which did not alter his condition. A senior resident reviewed the ECG at the bedside and obtained another ECG at double-standard amplitude (Figure 2). Sinus P waves were noted throughout the ECG, and no other atrial activity, such as retrograde P waves or flutter waves, was seen. All QRS complexes showed a baseline right bundle-branch block, all preceded by P waves. Because the arrhythmia started suddenly (as was evidenced by the telemetry strip, which is no longer available, but which showed a sinus rhythm at 60 beats/min immediately before onset) a presumptive diagnosis of sinoatrial nodal reentry tachycardia was made, and the patient was treated with 2.5 mg of IV metoprolol (Lopressor). Shortly after administration, his heart rate abruptly dropped to 65 beats/min (Figure 3), and a new ECG confirmed the rhythm to be sinus. Although an ectopic atrial tachycardia may have been the cause of this patient's arrhythmia, it was considered less likely because of the sinus morphology of the P wave.

Figure 1—The patient's ECG, showing discrete sinus P waves (arrows).

Figure 2—A subsequent ECG at double-standard amplitude more clearly identifies the sinus P waves (arrows).

Figure 3—Rhythm tracing at the moment of conversion from sinoatrial node reentry to normal sinus rhythm (arrows identify the P waves).

The patient was soon discharged back to the nursing facility in sinus rhythm, without further complications.

Diagnosis

All sinus tachycardias present with sinus P waves on the surface ECG, so the correct diagnosis depends greatly on the clinical scenario. For all hemodynamically stable patients, a 12-lead ECG should be evaluated for the presence and morphology of P waves. The absence of P waves usually denotes a junctional tachycardia or an atrioventricular (AV) nodal reentry tachycardia. In patients with a rapid heart rate, it is not unusual to confuse a T wave from a preceding beat with a P wave from a following beat; therefore, particular attention should be paid to morphology, to avoid this potential pitfall.

The findings of "atypical" or retrograde P waves are consistent with AV reentry tachycardia. These atypical waves should be evaluated closely to avoid confusion with the classic sawtooth pattern that is usually associated with atrial flutter. Often, when sinus P waves are found, the diagnosis of sinus tachycardia is made, but further information may be required to ascertain the origin of the rapid heart rate.

Differentiating between the sinus tachyarrhythmias carries important therapeutic and prognostic implications. The principal characteristics of sinus tachyarrhythmias are summarized in the Table.⁵

An adequate history (or a telemetry strip, if available) should be obtained in an effort to differentiate between sudden-onset and gradual-onset tachycardias. Abrupt onset is usually associated with reentry patterns and may be preceded by premature atrial contractions. If the tachyarrhythmia had a gradual onset, further clinical information may elucidate the cause. For example, the presence of fever, hypoxia, or blood loss makes the diagnosis of appropriate sinus tachycardia almost certain. If there is suspicion of an association with the patient's postural changes, the diagnosis of postural orthostatic tachycardia syndrome should be considered, and may be elicited at the patient's bedside using classic orthostatic maneuvers.

Differentiating between the
sinus tachyarrhythmias carries
important therapeutic and
prognostic implications.

Regardless of the results of the bedside evaluation, if there is still clinical suspicion of postural orthostatic tachycardia, the patient should undergo a tilt-table test. The diagnosis of inappropriate sinus tachycardia can be made by excluding drugs, endocrine abnormalities, and other significant medical comorbidities. Finally, if the tachycardia presents—and maybe even terminates—abruptly, sinoatrial nodal reentry tachycardia should be considered.

Sinoatrial Nodal Reentry Tachycardia

The incidence of sinoatrial nodal reentry tachycardia has been estimated at between 2% and 17% among individuals undergoing electrophysiologic study for supraventricular tachycardia.³ The etiology of sinus reentry tachycardia has not been fully clarified, and there are several competing hypotheses.⁴ The discrepancy in the nomenclature (ie, sinoatrial nodal versus sinus reentry tachycardia) stems from disagreement as to the precise anatomic and physiologic bases of the arrhythmia. Animal studies have suggested that it is strictly inside the sinus node, but this has yet to be proved conclusively.

Sinoatrial nodal reentry tachycardia can be initiated by atrial premature beats, atrial pacing, and, unlike intraatrial reentry, by ventricular premature beats and ventricular pacing with retrograde ventriculoatrial conduction. Once the arrhythmia begins, the electrical current conducts around (or inside) the sinus node in an organized manner, causing regular atrial and ventricular contractions. The atrial stimulation, as seen on a surface ECG, will be identical to that of physiologic sinus tachycardia.⁶

Patients with sinoatrial nodal reentry tachycardia may be symptomatic,³ often presenting with palpitations and diaphoresis. The condition is not as benign as previously believed, and it tends to be found in patients with organic heart disease. Patients should be treated promptly upon diagnosis.

Treatment

Even though the Advanced Cardiac Life Support protocol suggests the use of IV adenosine (Adenocard IV, Adenoscan) as a first-line treatment for stable narrow-complex tachycardias, this agent has not been shown to be more effective than other pharmacotherapies, such as a calcium channel blocker, a beta-receptor antagonist, or IV amiodarone HCl,⁵ for the treatment of sinoatrial nodal reentry tachycardia. Beta antagonists are considered first-line therapy in most sinus tachyarrhythmias (except for appropriate sinus tachycardia), and even though no controlled trials have been reported, it stands to reason that their use should not be precluded in hemodynamically unstable patients if the arrhythmia is thought to be the cause rather than the consequence of the instability.

Specific bradycardic agents derived from verapamil (as well as from clonidine) are in the investigational phase, but their development has been hampered by adverse drug reactions.⁷

Treatment of recurrent and sustained sinoatrial nodal reentry tachycardia with radiofrequency ablation has been reported by different centers to carry a high success rate and few complications; it should be considered in very select patients, such as those with recurrent symptomatic episodes that do not respond to medical therapy.^7-9

No studies are available on the long-term outcomes of patients with sinoatrial nodal reentry tachycardia. A single study has looked into prognostic markers for successful ablation, but it did not provide any longterm follow-up data.¹⁰ Based on the available data, appropriate therapy (such as bedside maneuvers, medication, or ablation) is associated with an acceptable short- and medium-term prognosis.

Conclusion

It is important to distinguish sinus tachycardias from other narrow-complex tachycardias, because management differs for each. When the onset is abrupt, the arrhythmia is symptomatic and has no obvious cause, and the ECG is consistent with sinus tachycardia, it is important to consider less-common diagnoses, such as sinoatrial nodal reentry tachycardia. Events can often be terminated using vagal maneuvers, IV adenosine or amiodarone, calcium channel blockers, or beta-receptor antagonists. When the condition persists, some patients may require radiofrequency catheter ablation.

SELF-ASSESSMENT TEST

1. Which of the following statements about sinus tachycardias is true?
   
   
   1. They all present with sinus P waves on surface ECG
   2. They are the least common type of arrhythmia
   3. Retrograde P waves suggest sinoatrial reentry tachycardia
   4. Fever suggests inappropriate sinus tachycardia


2. Which one of the following narrow-complex tachycardias is not associated with sudden onset?
   
   
   1. Sinoatrial node reentry
   2. AV nodal reentry
   3. Multifocal atrial
   4. Atrial flutter


3. Which of the following statements about sinoatrial node reentry tachycardia is not true?
   
   
   1. Patients may be asymptomatic
   2. It is often associated with organic heart disease
   3. The ECG will show variable P waves
   4. It has an abrupt onset


4. Which of these characteristics is not typical of sinoatrial node reentry tachycardia?
   
   
   1. Heart rate increases in upright position and decreases with recumbency
   2. Heart rate >100 beats/min
   3. Paroxysmal tachycardia
   4. Initiation by premature stimuli


5. All the following medications are appropriate IV treatments for sinoatrial node reentry tachycardia, except:
   
   
   1. Amiodarone
   2. Verapamil
   3. Adenosine
   4. Lidocaine

(Answers at end of references list)

References

1. Delacrétaz E. Supraventricular tachycardia. N Engl J Med. 2006;354:1039-1051.
2. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31:150-157.
3. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary. J Am Coll Cardiol. 2003;42:1493-1531.
4. Yusuf S, Camm AJ. The sinus tachycardias. Nat Clin Pract Cardiovasc Med. 2005;2:44-52.
5. Yusuf S, Camm AJ. Sinus tachyarrhythmias and the specific bradycardic agents: a marriage made in heaven? J Cardiovasc Pharmacol Ther. 2003;8:89-105.
6. Gomes JA, Mehta D, Langan MN. Sinus node reentrant tachycardia. Pacing Clin Electrophysiol. 1995;18:1045-1057.
7. Kay GN, Chong F, Epstein AE, et al. Radiofrequency ablation for treatment of primary atrial tachycardias. J Am Coll Cardiol. 1993; 21:901-909.
8. Sanders WE Jr, Sorrentino RA, Greenfield RA, et al. Catheter ablation of sinoatrial node reentrant tachycardia. J Am Coll Cardiol. 1994;23:926-934.
9. Lesh MD, Van Hare GF, Epstein LM, et al. Radiofrequency catheter ablation of atrial arrhythmias. Results and mechanisms. Circulation. 1994;89:1074-1089.
10. Ivanov MY, Evdokimov VP, Vlasenco VV. Predictors of successful radiofrequency catheter ablation of sinoatrial tachycardia. Pacing Clin Electrophysiol. 1998;21:311-315.

Answers: 1. A; 2. C; 3. C; 4. A; 5. D.