The Other Sinus Tachycardias

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. The arrhythmia is characterized by a resting heart rate over 100 bpm or a heart rate that increases to over 100 with just minimal exertion or as a response to stress. The heart rate may drop into the 80s during sleep. The P wave seen is the same as in normal sinus rhythm. The onset and termination of the rhythm are gradual. The rhythm is noninducible in the EP lab, and responds to carotid sinus massage with slowing but not termination.2 Patients correlate their symptoms with actual documentation of the tachycardia. Differential diagnoses may include right atrial tachycardia and postural orthostatic tachycardia syndrome (POTS). IAST seems to occur most often in young women aged 15-50.4,5 Symptoms include palpitations, dizziness, syncope, orthostatic intolerance, chest pain, headache, myalgia, dyspnea, anxiety, depression, reduced exercise tolerance, and abdominal discomfort. Symptoms may be present for months or years. Some cases have followed a viral illness or physical trauma. The two theories that have been proposed for the etiology of the rhythm are excessive autonomic tone or abnormal sinus node function. The excessive autonomic tone or dysautonomia hypothesis suggests that there is a loss of autonomic balance, with either the sympathetic dominating or the parasympathetic being blunted. It is important to keep in mind that dysautonomias are often inherited. The abnormal sinus node function hypothesis suggests that the SA node may be structurally abnormal, leading to an enhanced heart rate response to epinephrine.6 Ultimately these abnormalities both lead to a loss of heart rate variability. Treatment options include ablative and noninvasive approaches. The ablative approach to management involves modification of the SA node. After ablation, immediate response may be favorable, but long-term success rates have been disappointing.5-7 The noninvasive management includes avoidance of possible event triggers. Antiarrhythmic drugs that have been found useful include beta-blocking agents, calcium-channel blockers, and class IC agents. Because of the autonomic trigger mechanism that may be responsible for initiation of the tachycardia episodes, adjunctive therapies such as aerobic training, biofeedback, and meditation, which aim to decrease the sympathetic component, are also being tried. Postural Orthostatic Tachycardia Syndrome (POTS) Postural orthostatic tachycardia has been included in a symptom complex of exercise intolerance, dizziness, fatigue, near-syncope, and visual blurring. This grouping of symptoms is known as postural orthostatic tachycardia syndrome. In some cases these symptoms have also been linked to chronic fatigue syndrome. The criteria for POTS includes: a heart rate increasing 30 bpm or more and a heart rate of 120 bpm or more within 10 minutes of standing or tilt; symptoms of orthostatic intolerance; no known autonomic neuropathy; and a serum norepinephrine level greater than 600 pg/ml.8 There are also some POTS cases in which features overlap with those of IAST.4,9 A variety of mechanisms have been proposed for POTS. One is that of a mild form of peripheral autonomic neuropathy in which peripheral vasculature does not constrict adequately during orthostatic stress. This form is seen in patients between the ages of 14 and 50, and more frequently in females. The second form is manifested by beta-adrenergic receptor sensitivity. Some forms of POTS are also linked to other known syndromes.8 Clinical experience and knowledge of prognosis for POTS is limited, but it’s generally believed that the younger the age at onset, the greater the chance for recovery. The workup should include a detailed history; blood pressure and heart rate measured in supine, sitting, and standing positions; electrocardiogram; echocardiogram; tilt study; and plasma norepinephrine levels. Treatment includes identification and avoidance of reversible causes of volume depletion, elimination of drugs that cause dehydration or venous pooling, increase in sodium and fluid intake, exercise, support hose, and cognitive-behavioral interventions. Drugs that may be prescribed (depending on the suspected mechanism) include fludrocortisone (volume expansion), midodrine (peripheral alpha-receptor stimulator), labetalol (beta-blocker), yohimbine (alpha-agonist), erythropoietin (volume expansion), venlafaxine (reduction of anxiety), methylphenidate (amphetamine/vasoconstrictor), pyridostigmine (acetylcholinesterase inhibitor), phenobarbital (reduction of anxiety), vasopressin (volume expansion), clonidine (alpha-agonist), and octreotide (vasoconstrictor). Summary Sinus tachycardia, though seemingly not as exotic a diagnosis as many that are encountered in cardiac electrophysiology, can offer many challenges. An increased awareness of the various mechanisms responsible will lead to a speedier diagnosis and treatment for our patients.