The sinoatrial node (SA) is crescent in shape and is located in subepicardially. It is 13.5 millimeters in length and is innervated by vagus and sympathetic nerves in an average adult. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases it comes from the left circumflex coronary artery. The SA node is a crucial component of the hearts conduction system and is its default pacemaker.
Sinoatrial nodal reentrant tachycardia is a rare form of paroxysmal supraventricular tachycardia that has the following electrocardiogram features:
The American College of Cardiology/American Heart Association Task Force on clinical practice guidelines and the heart rhythm society has defined sinoatrial nodal reentrant tachycardia as a focal atrial tachycardia from micro-reentry arising from the sinus node.
The exact mechanism of sinoatrial nodal reentrant tachycardia remains controversial. There are 3 distinct mechanisms which are possible.
Most evidence suggests that the reentry circuit usually involves either just the sinoatrial node or both the sinoatrial node and the perinodal tissue. Theory of the sinoatrial node as a refractory center seems to lack much evidence.
Although common in children and adults, who have structural heart disease SANRT is considered an uncommon tachyarrhythmia with very rare symptomatic presentations. In an electrophysiologic study on patients with paroxysmal supraventricular tachycardia incidence of SANRT was found to be within 2% to 17%. The exact prevalence of SANRT is difficult to determine both in the United States and globally as patients with this arrhythmia do not usually have symptoms and therefore do not present for electrophysiology study. Also since SANRT is very similar to sinus tachycardia on the electrocardiogram, it is underdiagnosed.
SANRT, as discussed, is prevalent among patients who have structural heart disease. The exact structure of the reentry circuit is controversial but is mostly believed to exist just within the SA node itself or to involve the perinodal tissue together with the SA node for the manifestation of this tachyarrhythmia. No extrinsic factors are known to cause SANRT.
Histopathological features of the reentrant circuit in humans are yet to be studied although one study in dogs showed that increased intranodal fibrosis post myocardial infarction provided an increased substrate for SANRT.
Patients with SANRT are usually asymptomatic. In rare cases, patients might present with symptoms of intermittent palpitations secondary to abrupt onset and cessation of the rhythm. Other symptoms patient might present with include dizziness, shortness of breath, pain/discomfort in the neck, pain/discomfort in the chest, anxiety, and polyuria secondary atrial natriuretic factor secreted mainly by the heart atria in response to atrial stretch. Although, uncommon patients with SANRT and known history of coronary artery disease may present with a myocardial infarction secondary to the stress on the heart. Patient with SANRT and known history of heart failure may come in with acute exacerbation with possibly reduced ejection fraction secondary to tachycardia-induced cardiomyopathy.
Patients with SANRT usually present with a heart rate within the range of 100 to 150 bpm. If a patient has known heart failure or coronary artery disease, he may complain of chest pain and may also have symptoms of heart failure such as wheezing or swelling in the lower extremities and tachypnea on physical exam. In rare instances, patients with SANRT might present with complaints of syncope secondary to tachycardia-induced reduced ventricular filling as less filling of the ventricles leads to the reduction in the cardiac output which leads to decreased perfusion of the brain. Tachycardia-induced depression of the sinoatrial node may also contribute to syncopal symptoms. Hypotension secondary to decrease ventricular filling may be a significant physical exam finding in patients presenting with SANRT.
The most significant component of the assessment for a patient who presents with signs and symptoms of sinoatrial nodal reentrant tachycardia is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate) and an electrocardiogram. A patient presenting with SANRT should undergo evaluation for any unknown underlying coronary artery disease or heart failure. During an assessment, it should be established whether the patient is hemodynamically stable based mainly on his blood pressure, mental status, and respiratory rate. Initial evaluation of patients with SANRT can include testing to access the patient's thyroid and pulmonary function, together with routine blood work. Since there is a frequent association between SANRT and structural heart disease part of patients evaluation might also include echocardiography.
Most patients with SANRT do not need medical intervention as a heart of 100 to 150 bpm rarely induces any symptoms. In rare cases, patients with frequent SANRT might develop symptoms and require medical management. These patients might also benefit from treatment to avoid long-term adverse effects such as tachycardia-induced cardiomyopathy.
Medical management of patients presenting with SANRT begins with an initial evaluation of their hemodynamically stability. Hemodynamically unstable patients present with tachycardia associated with hypotension, ischemic chest pain, altered mental status, respiratory failure, or shock and these patients need their SANRT terminated electrically with an urgent electrical cardioversion. Hemodynamically stable patients should be treated first with a carotid massage or other such vagal maneuvers to cease the rhythm acutely. If such methods are ineffective or inappropriate, intravenous adenosine is the next best step in the absence of contraindications to adenosine.
Currently, there is lack of large pharmacological studies in patients who present with SANRT due to the rarity of the rhythm and its less frequent complications. For chronic suppression of recurrent SANRT radiofrequency catheter ablation is recommended rather than suppressive medical therapy due to higher success rates of ablations together with short and long-term side effects of the medications. However, in patients who require prolonged suppressive medical therapy, verapamil, digoxin, or amiodarone can be used.
As a result of extensive autonomic innervation of the sinus node, Valsalva maneuvers tend to terminate SANRT abruptly in contrast to sinus tachycardia where Valsalva maneuvers result in gradual slowing and then a gradual acceleration of the rhythm upon stopping of such maneuvers.
SANRT is a rare arrhythmia but can be confused with other atrial arrhythmias. Healthcare workers including the nurse practitioner should carefully examine these patients and rule out other reversible causes. Patients should be referred to a cardiologist if there is any echo evidence of structural heart disease. Most patients with SANRT do not need medical intervention as a heart of 100 to 150 bpm rarely induces any symptoms. In rare cases, patients with frequent SANRT might develop symptoms and require medical management. These patients might also benefit from treatment to avoid long-term adverse effects such as tachycardia-induced cardiomyopathy.
Currently, there is lack of large pharmacological studies in patients who present with SANRT due to the rarity of the rhythm and its less frequent complications. For chronic suppression of recurrent SANRT radiofrequency catheter ablation is recommended rather than suppressive medical therapy due to higher success rates of ablations together with short and long-term side effects of the medications. However, in patients who require prolonged suppressive medical therapy, verapamil, digoxin, or amiodarone can be used. (Level V)
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