AV node reentry tachycardia: The basics and more advanced:
What is supraventricular tachycardia (SVT)? — Supraventricular tachycardia, also called “SVT,” is a heartbeat that is faster than normal. It usually starts and stops suddenly, without warning. SVT is also called “paroxysmal supraventricular tachycardia” or PSVT. (Paroxysmal means a sudden attack.)
SVT happens because of a problem with the heart’s electrical system. It starts in the upper chambers of the heart, called the “atria” (figure 1). The fast heartbeat can last from a few minutes to hours, but usually lasts for 10 to 15 minutes. It often happens when you are at rest. But in some people, exercise triggers it.
The 3 main types of SVT are called:
●Atrioventricular nodal reentry tachycardia (AVNRT)
●Atrioventricular reentry tachycardia (AVRT)
What are the symptoms of SVT? — You might not have symptoms. But you might feel that your heart is beating too fast, beating hard, or seems to skip a beat. These kinds of heartbeat changes are called “palpitations.”
You might also feel:
If you also have coronary heart disease, you might also:
●Have trouble breathing
●Feel a tightness in your chest
Should I see a doctor or nurse? — If you have trouble breathing or have chest pain, call Dr. Uri Ben-Zur at 818-483-3832 or dial 911. Dr. Ben-Zur is the best cardiologist in Los Angeles and can assist you on any issue that you may have with your heart. If you are concerned that you may be at risk, schedule an appointment today so we can keep your heart strong and healthy.
If you do not have these problems, but you often feel your heart beating fast or irregularly, talk to your doctor or nurse.
Is there a test for supraventricular tachycardia? — Yes. Your doctor or nurse will do a test called an electrocardiogram, also known as an “ECG” or “EKG.” This test measures the electrical activity in your heart.
Other possible tests include:
●Holter monitor – This is a small, portable machine you wear that records all the heart’s electrical activity over 1 or 2 days.
●Event or loop monitor – These are similar to Holter monitors but smaller, because they don’t record all the time. Instead, you start the monitor when you feel symptoms. Your doctor will likely have you wear one of these monitors every day for about a month.
How is supraventricular tachycardia treated? — The treatment depends on the cause of the tachycardia. When your heartbeat is very fast, your doctor might suggest ways to slow it down. He or she might have you cough, or bear down as if you’re having a bowel movement. He or she might also suggest that you put an ice pack on your face. Doing these things can affect the nerve that helps control your heartbeat.
Other treatments can include:
●Medicines to control the speed or rhythm of your heartbeat
●A treatment called “cardioversion” that involves applying a mild electrical current to the heart to fix its rhythm
●Treatments called “ablation.” Ablation treatments use heat (called “radiofrequency ablation”) or cold (called “cryoablation”) to destroy the small part of the heart that is sending the abnormal electrical signals.
P wave is falling below the QRS complex
Atrioventricular nodal reentrant tachycardia (AVNRT) is one of the common supraventricular tachycardias (SVTs). As with the majority of SVTs, the QRS complex in AVNRT is usually narrow (ie, ≤120 msec), reflecting normal ventricular activation through the His-Purkinje system. There are a number of synonyms for AVNRT, including:
●AV nodal reentry
●Reciprocal or reciprocating AV nodal reentrant tachycardia
●Junctional reciprocating tachycardia
Symptoms — the symptoms associated with arrhythmia episodes are nonspecific. The nature and severity of symptoms are often influenced by the rate of the tachycardia. Because of the paroxysmal nature of the arrhythmia, the onset and termination of the symptoms are usually sudden.
Patients most commonly complain of palpitations, an odd feeling in the chest, and, on occasion, lightheadedness. Those with significant heart disease may have additional symptoms such as dyspnea and chest pain. Some patients with AVNRT have a feeling of polyuria and experience a diuresis during or after AVNRT; the mechanism probably is related to an elevated mean right atrial pressure and plasma level of atrial natriuretic peptide, which are present during the arrhythmia .
V nodal reentry presents with the following symptoms and frequencies:
●Palpitations – 98 percent
●Dizziness – 78 percent
●Dyspnea – 47 percent
●Chest pain – 38 percent
●Fatigue – 19 percent
●Syncope – 16 percent
Dual AV nodal physiology — the simplest concept of AV nodal physiology that allows for reentry involves separate electrical pathways within or proximal to the AV node.
●One pathway conducts rapidly and has a relatively long refractory period. This is called the fast pathway (common).
●The second pathway conducts relatively slowly and has a shorter refractory period. This is called the slow pathway (uncommon).
See these Youtube videos for more information with visual references:
The origins of the fast and slow pathways are probably in perinodal atrial tissue. These pathways join and enter a final common pathway in the AV node. While atrial tissue above the AV node appears to be part of the reentrant circuit, the bundle of His below the node is probably not a necessary part of the circuit. This can be illustrated by the following observations:
●AVNRT is associated with 2:1 AV block in approximately 10 percent of patients . With this form of block, the completion of two complete circuits is evidenced by two retrograde P waves while only one of the impulses traverses the His bundle on the way to the ventricles. Thus, the bundle of His is not a required component of the circuit. The AV block in this setting is probably a functional infranodal block within the bundle of His.
General features — The usual electrocardiographic features of AVNRT include the following:
●The rate is generally between 120 and 220 beats/minute.
●In the common form, retrograde atrial activation and anterograde ventricular activation occur almost simultaneously. The P wave, therefore, is usually buried within or fused with the QRS complex. A component of the P wave is often evident slightly after, or less commonly before, the QRS. When the P wave occurs shortly after the QRS complex, the fused waveform can produce a pseudo-R’ (a second R wave) in lead V1 and a pseudo-S wave in the inferior leads.
●If the initiation of the tachycardia is captured on a tracing, the tachycardia often begins with a premature atrial depolarization with sudden prolongation of the PR interval.
●In the uncommon form of AVNRT, retrograde atrial activation occurs long after ventricular activation, resulting in a P wave so late after the QRS complex that it appears to be occurring shortly before the next QRS complex. This pattern resembles that seen in atrial tachycardias. In such cases, an EP study may be required to define the arrhythmogenic mechanism.
Because of the relationships between the QRS complex and the following P wave, the common form of AVNRT is referred to as a “short RP tachycardia,” while the uncommon form is a “long RP tachycardia.”
P wave morphology — The axis of the P wave, when seen, is abnormal due to retrograde atrial activation. This is usually manifested on the electrocardiogram by inverted P waves in leads I, II, III and aVF. In atypical AVNRT, however, the P wave is generally upright or isoelectric in lead I.
ST segment depression — Significant ST segment depression during tachycardia has been observed in 25 to 50 percent of patients with AVNRT, although it is more commonly seen in those with an AV reentrant tachycardia associated with an accessory pathway. Although the presence of ST segment depression suggests myocardial ischemia, the majority of patients do not have underlying coronary artery disease; in these patients ST segment changes represent either repolarization changes or a retrograde atrial activation.
T wave inversions after termination — After acute termination of AVNRT and other paroxysmal SVTs, T wave inversions may be seen in the anterior or inferior leads. In a series of 63 patients with paroxysmal SVT, such abnormalities were present in about 40 percent of patients. They may be seen immediately upon AVNRT termination or may develop within the first six hours, and can persist for a variable duration (mean of 34 hours). The occurrence of negative T waves is not predicted by clinical parameters, tachycardia rate or duration, or the presence and extent of ST segment depression during the tachycardia. They are not the result of coronary artery disease, but are repolarization abnormalities, likely due to ionic current alterations resulting from the rapid rate.
THERAPY — The general approach to the therapy of AVNRT includes two components, acute termination of the arrhythmia and prevention of recurrent episodes.
Acute termination — The recommended approach to acute termination of AVNRT depends upon the severity of the arrhythmia.
Hemodynamic collapse or severe symptoms — Severe hemodynamic decompensation is uncommon in AVNRT. Hemodynamic compromise may be manifested clinically by one or more of the following features:
●Hypotension and shock
●Shortness of breath and/or heart failure
●Syncope or near-syncope
In such cases, immediate restoration of normal sinus rhythm is essential. Based upon their speed of onset and high therapeutic efficacy, treatment options in this setting include:
●DC Stable patient — There are few data regarding the optimal approach to the acute termination of AVNRT. Management recommendations are based upon an understanding of the properties and risks of the treatment options. In 2003, the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) published guidelines for the management of patients with supraventricular arrhythmias, which included recommendations on the acute treatment of AVNRT . Our recommendations are in general agreement with those guidelines.
In patients who are hemodynamically stable, whether symptomatic or asymptomatic, we suggest the following approach to acute termination of the arrhythmia:
●Vagal maneuvers (eg, Valsalva maneuver or carotid sinus massage) — Vagal maneuvers increase parasympathetic tone, which produces a gradual slowing of conduction in the antegrade slow pathway. Slowing and eventual block in the antegrade slow pathway are the usual cause for arrhythmia termination with these interventions, although they can also produce abrupt block in the retrograde fast pathway. Vagal maneuvers are less effective in hemodynamically unstable patients, since this state is typically characterized by increased sympathetic tone and parasympathetic withdrawal.
●Adenosine — If vagal maneuvers cannot be performed or if they fail to terminate the arrhythmia, adenosine is usually the first pharmacologic agent administered. The advantages of adenosine over other agents include rapid onset and a short half-life. Adenosine terminates AVNRT in over 80 percent of cases. It is well tolerated in most patients, with the exception of those with severe bronchospastic asthma or severe coronary artery disease. Detailed discussions of the use of adenosine for the evaluation and termination of SVTs are presented separately.
●Nondihydropyridine calcium channel blockers — If adenosine is ineffective, intravenous verapamil and diltiazem can be used to terminate AVNRT. These drugs are generally well-tolerated, although potential adverse effects include hypotension (due to both negative inotropic and vasodilatory effects) and bradycardia.
●Beta blockers — Intravenous beta blockers (eg, metoprolol, esmolol), are alternatives to verapamil or diltiazem in patients who do not respond to or are intolerant of adenosine. Similar to the calcium channel blockers, beta blockers have the potential to cause hypotension and/or bradycardia, and therefore they should be used cautiously, particularly if calcium channel blockers have already been administered.
Because of their longer half-lives, verapamil, diltiazem, and beta blockers have the potential to suppress arrhythmia recurrence. Thus, these drugs should be used in patients who have early arrhythmia recurrence after termination with adenosine.
Pill-in-the-pocket — In selected patients with infrequent, well-tolerated, and long lasting episodes of AVNRT, a single dose of an antiarrhythmic agent that was previously evaluated under observation can be effective for acute termination of the arrhythmia. This strategy can both reduce the need for emergency department visits and avoid chronic medical therapy or invasive procedures. This approach has been evaluated with the nondihydropyridine calcium channel blockers, beta blockers, and the class IC antiarrhythmic drug flecainide. However, based upon the efficacy of alternative, lower-risk therapies, flecainide is rarely used in the management of AVNRT.
Chronic therapy — Not all AVNRT patients require long-term suppressive therapy. The decision to treat is based upon the following factors:
●The frequency of the arrhythmia
●The significance of the symptoms
●Patient tolerance of medications
Patients with symptomatic and/or frequent episodes of AVNRT are generally treated with either catheter ablation or chronic suppressive pharmacologic therapy. There are few data to guide the selection of a specific therapy, and choices are influenced by patient preference. The 2003 ACC/AHA/ESC guidelines on the management of supraventricular arrhythmias included recommendations for the chronic therapy of AVNRT, and as with acute therapies, our recommendations are in general agreement with those guidelines.
No treatment — Patients with infrequent and well-tolerated episodes of AVNRT may choose no chronic therapy. Such patients can be taught to terminate the arrhythmia using safe vagotonic maneuvers, particularly the Valsalva maneuver and its variants.
Pharmacologic therapy — There are few data comparing the relative efficacy of various agents. Because they are effective and well tolerated, the medications that are most commonly used for the chronic suppression of AVNRT are the nondihydropyridine calcium channel blockers verapamil and diltiazem, and ß-blockers.
Among patients who do not respond to diltiazem, verapamil or ß-blockers and who do not want to pursue EP study and ablation, the following antiarrhythmic drugs may be considered:
●Flecainide (class IC)
●Propafenone (class IC)
●Sotalol (class III)
●Amiodarone (class III)
However, due to the potential for significant toxicities, including proarrhythmia, the use of class I and class III antiarrhythmic drugs for the management of AVNRT should be reserved for rare cases and should be administered in consultation with an electrophysiologist. In particular, because of the risk of toxicities with long-term use, amiodarone is usually avoided in young patients.
Catheter ablation — Catheter ablation offers the opportunity for definitive control of the arrhythmia and the avoidance of chronic medical therapy. However, ablation incurs the risks of procedural complications, including a 1 percent risk of heart block requiring a pacemaker. Due to its favorable efficacy and safety profile, this option is increasingly favored among patients with recurrent AVNRT.
The general approach to the catheter ablation of AVNRT is based upon the concept of dual AV nodal pathways. The most common AVNRT circuit (80 to 90 percent) involves antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. The most common ablation target is the posterior slow pathway (figure 8) since ablation here carries the lowest risk of AV block, preserves fast pathway function (and a normal PR interval post-ablation), and is facilitated by reliable anatomic and electrophysiologic landmarks. The anterior fast pathway can also be ablated, but this approach is now limited to a few special circumstances since fast pathway ablation results in a long PR interval during sinus rhythm and is associated with a higher risk of heart block.
In the hands of experienced operators, the posterior approach eliminates arrhythmia recurrence in over 95 percent of patients. Evidence of dual pathway physiology can persist in one-third to one-half of cases, but it is not necessary to eliminate all slow pathway conduction to achieve clinical success (ie, elimination of arrhythmia recurrence).
The anterior approach to ablation targets the fast pathway in the anterior third of Koch’s triangle, somewhat anterior and proximal to the His Bundle. Although the success rate rivals the posterior approach, the risk of creating complete AV block with ablations in this area is higher than in the posterior third of Koch’s triangle. The anterior approach is now limited to unusual circumstances, such as patients with a previously unsuccessful posterior pathway ablation or those with a markedly prolonged baseline PR interval and absent antegrade fast pathway conduction in whom posterior pathway ablation may result in complete heart block and the need for a permanent pacemaker.
The most significant potential complication of RFA for AVNRT is AV block. Complete AV block is less common (about 1 percent, range 0 to 3 percent) with the posterior than the anterior approach. Older age and baseline PR interval prolongation are predictors of an increased risk of post-ablation AV block.
AV block may not be immediately observed, but may progress following the procedure. However, this is extremely rare in patients who did not have transient AV block during the ablation. The use of cryothermal ablation of the slow pathway is an approach that may reduce the potential for AV block; the ability to test prospective ablation sites before permanent destruction can prevent this inadvertent complication.
Catheter ablation in patients with cardiac implantable electronic devices — On occasion, catheter ablation is performed in patients who have a permanent pacemaker or implantable cardioverter-defibrillator (ICD). While transient elevations in pacing thresholds and diminished electrograms may be observed, these changes are rarely persistent or prolonged.
Pharmacologic therapy versus ablation therapy — AVNRT is usually well-tolerated, and a variety of treatment options are safe and effective. Thus, in the absence of compelling data favoring one therapy over another, the choice of chronic treatment strategies is influenced by patient preference.
The relative efficacy and costs of catheter ablation and medical therapy were compared in a series of 79 patients with newly documented SVT who were treated with either ablation or pharmacologic therapy, based upon patient preference. After a follow-up period of 12 months, both medication and ablation decreased the frequency of arrhythmia-related symptoms, but ablation was more likely to result in complete abolition of symptoms (74 versus 33 percent). Although ablation was initially more costly, the potential long-term costs were estimated to be similar after 9 to 12 years because of the cumulative cost of pharmacologic therapy.
Generally speaking, catheter ablation and medical therapy are comparable in both cost and efficacy, with ablation particularly useful in patients with frequent symptomatic episodes. Most of these studies evaluated patients with drug-refractory AVNRT, a population in whom catheter ablation would be expected to perform well. However, catheter ablation may also be cost-effective as initial therapy for patients with paroxysmal AVNRT.
When working with a patient to select a treatment strategy, the following issues should be considered:
●Many patients with well-tolerated symptoms prefer a more conservative initial approach, with either no specific therapy or pharmacologic suppression.
●If pharmacologic therapy fails or if the side effects of chronic medications are poorly tolerated, patients often prefer EP study and ablation.
●For patients who prefer definitive therapy, even for rare, well-tolerated episodes, catheter ablation is a reasonable option.
●For patients with episodes of AVNRT that are poorly tolerated (eg, associated with near-syncope or syncope, angina, or severe dyspnea), we suggest catheter ablation as initial therapy. In such cases, the risks associated with recurrent arrhythmic events (eg, syncope with associated trauma) outweigh the procedural risks. In addition, the potential for definitive therapy makes ablation preferable to medical therapy in this setting.