Advances in the field of cardiac electrophysiology have uncovered multiple mechanisms that may be responsible for the presence of sinus tachycardia. These various forms were only hinted at 20 years ago. This article is a review of what we currently know.

Sinus Tachycardia (ST)

The sinus tachycardia that we know best is a physiologic response to the need of the body for increased heart rate.1 This response may be caused by fever, increased activity, increased sympathetic tone, or metabolic imbalances. ST may also be a compensatory response to decreased ejection fraction in the setting of heart failure. The mechanism responsible for this ‘pure form’ is enhanced automaticity. ST is characterized by a gradual heart rate increase and gradual decrease with termination.

The response to carotid sinus massage is a temporary slowing, followed by resumption of the original rate.

The heart rate seen with ST will be in the range of 100-150, the P wave will be the normal sinus P wave, and the QRS will be of normal width. There is no specific drug used for termination of the rhythm. Treatment consists of identification of the cause of the rate increase and treating that. Figure 1 is an example of sinus tachycardia.

SA Node Reentry Tachycardia (SANRT)

This is a rhythm that was originally proposed in the laboratory setting. To understand how SANRT occurs, it is helpful to look at anatomy. Many textbook figures portray the SA node as a globular structure; however, the SA node is actually shaped like a comma. Understanding the true shape and breadth of the node makes it easier to conceptualize a reentry tachycardia from the node (Figure 2). SANRT occurs because of an area of slow conduction within a region of the node, allowing reentry to occur. SANRT will look like sinus tachycardia once it has begun. The P wave will look like the normal sinus P or could be upright in leads II, III and AVF.2 The crucial feature in SANRT identification is that the arrhythmia is paroxysmal, with sudden onset and sudden termination. The tachycardia can be terminated with vagal maneuvers, adenosine, or a premature beat. It is also easily induced in the EP lab. Figure 3 is a rhythm strip that shows an SANRT termination; notice the P wave is the same in tachycardia as in the sinus rhythm that follows.

Patients who have SA node reentry may be symptomatic, complaining of palpitations, shortness of breath and other symptoms characteristic of paroxysmal tachycardias. However, unlike patients with other supraventricular tachycardias, those with SANRT rarely have a heart rate that exceeds 150 bpm. Highly symptomatic patients may be treated by SA nodal modification. Patients refusing ablation could be tried on antiarrhythmic agents. SANRT is sometimes classified as an automatic atrial tachycardia.3 Table 1 compares the characteristics of each type of sinus tachycardia.

Inappropriate Sinus Tachycardia (IAST)

IAST is a form of focal atrial tachycardia that originates from the superior aspect of the crista terminalis or terminal crest, in the sinus node region. Figure 4 shows an ‘atrial floor plan’ that demonstrates the relationship of structures within the atria. The crista terminalis can be seen in the right atrium. IAST has been difficult to classify; two theories exist for its origin, one being an abnormality of SA nodal function and the other possibly a dysautonomia.