Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common paroxysmal supraventricular tachycardia and is characterized by a reentrant mechanism within the atrioventricular node. This arrhythmia presents with sudden and regular episodes of tachycardia, with rates ranging from 140 to 250 bpm, and abrupt onset and termination. AVNRT is generally benign, but can cause significant symptoms such as palpitations, dyspnea, dizziness, and, rarely, syncope.
Its onset is related to the presence of a dual conduction pathway within the AV node, a congenital condition present in about 30% of the population. However, not all individuals with this characteristic develop the arrhythmia. The initiation of tachycardia is often linked to factors such as stress, physical exertion, electrolyte imbalances, or the intake of stimulants.
The diagnosis is based on the electrocardiogram (ECG), which during an episode shows a regular high-rate rhythm, without visible P waves or with retrograde P waves. Treatment involves terminating the acute episode through vagal maneuvers or antiarrhythmic drugs. In patients with recurrent episodes, catheter ablation offers a definitive solution with a high success rate.
AVNRT is due to the presence of a dual conduction pathway in the atrioventricular node, creating an electrophysiological substrate predisposed to the formation of a reentrant circuit. Under normal conditions, electrical impulses travel through a single conduction pathway. In subjects with dual AV nodal pathways, the node has two tracts with different characteristics:
When an atrial beat occurs while the fast pathway is still refractory, the impulse propagates only along the slow pathway. Once it reaches the lower AV node, the impulse may travel retrogradely via the fast pathway, creating a self-sustaining reentry circuit that results in tachycardia.
The trigger for AVNRT is often an atrial extrasystole that propagates unidirectionally along the slow pathway while the fast pathway remains refractory. This mechanism initiates a stable reentry that continues to stimulate atria and ventricles at a regular, rapid rate.
Persistence of the arrhythmia is promoted by factors that modulate AV nodal refractoriness. Increased sympathetic tone, due to stress, exercise, or anxiety, can reduce the refractory period of the fast pathway, increasing susceptibility to tachycardia. Electrolyte disturbances such as hypokalemia and hypomagnesemia can also facilitate perpetuation of the reentry circuit.
AVNRT is generally benign but may have hemodynamic repercussions in patients with underlying heart disease. During an episode, loss of atrioventricular synchrony may reduce ventricular filling and lead to decreased cardiac output. In patients with limited cardiac reserve, prolonged tachycardia may precipitate hemodynamic decompensation.
Another consequence of AVNRT is increased central venous pressure, due to atrial contraction simultaneous with ventricular systole. This can manifest as jugular venous distension and reduced systemic perfusion in predisposed individuals.
AVNRT is classified according to the direction of the reentry circuit and the sequence of nodal activation:
This form accounts for about 90% of cases. The reentry circuit is characterized by an impulse that initially propagates along the slow pathway and ascends via the fast pathway. On ECG, the tracing shows a short RP interval, less than 70 ms, with retrograde P waves hidden within the QRS complex or barely visible in the inferior leads.
This variant is less common and shows reversed conduction compared to the typical form. It is divided into two subtypes:
From an ECG perspective, atypical AVNRT is characterized by a longer RP interval, with more visible P waves compared to the typical form.
Atrioventricular nodal reentrant tachycardia (AVNRT) develops in individuals with an anatomical predisposition characterized by the presence of dual conduction pathways within the AV node. This condition is congenital and found in about 30% of the population, although only a subset of these individuals develop episodes of tachycardia. Onset is usually between 20 and 50 years, with a higher incidence in women than in men. The arrhythmia can appear sporadically or with varying frequency, depending on the presence of triggering factors.
Hyperactivation of the sympathetic nervous system plays a key role in modulating AVNRT. Factors such as stress, anxiety, and intense physical activity can lower the threshold for tachycardia initiation, facilitating activation of the reentry circuit. Electrolyte imbalances, particularly hypokalemia and hypomagnesemia, affect the electrical stability of the AV node and can increase susceptibility to arrhythmic episodes. Certain drugs, including beta-agonists and nasal decongestants, can act on the atrioventricular conduction system, making arrhythmia onset more likely in predisposed individuals.
Prevention of AVNRT relies on controlling predisposing factors and managing episodes. In patients with recurrent episodes, reducing the intake of stimulants such as caffeine and alcohol, and adopting stress management strategies (e.g., relaxation techniques or biofeedback) are recommended. For those with frequent AVNRT episodes, discontinuation of potentially proarrhythmic drugs and monitoring blood electrolyte levels to prevent arrhythmia-promoting imbalances are also advisable.
AVNRT presents with episodes of sudden, regular tachycardia, with a heart rate ranging from 140 to 250 bpm. Onset is typically paroxysmal, with abrupt beginning and end, without a phase of gradual acceleration or deceleration. Episodes can last from a few seconds to several hours, with individual variability in both frequency and duration.
Patients generally report rapid and regular palpitations, often accompanied by a sensation of strong, sudden heartbeats. In subjects with prolonged episodes, reduced cardiac output may cause dyspnea and a feeling of chest tightness, although these symptoms are not necessarily related to myocardial ischemia. In some cases, tachycardia may be associated with dizziness or presyncope, especially in patients with limited cardiac reserve or a tendency toward hypotension. Syncope is rare and mainly occurs in individuals with autonomic dysfunction or particularly prolonged, poorly tolerated episodes.
Many patients learn to recognize the triggers of their episodes, which may include physical exertion, intense emotions, or abrupt postural changes. Some report a sensation of pressure in the cervical region or bothersome pulsations in the jugular area, due to simultaneous atrial and ventricular contraction during tachycardia.
During an AVNRT episode, the most prominent finding is a rapid, regular pulse, with a ventricular rate typically between 140 and 250 bpm. Cardiac auscultation reveals tachycardic but rhythmic heart sounds, with no associated pathological murmurs. In patients with sustained tachycardia, reduced cardiac output may result in mild hypotension, although usually without signs of significant hemodynamic compromise.
A characteristic sign in AVNRT patients is the presence of prominent a waves on jugular venous pressure monitoring, caused by atrial contraction against a closed tricuspid valve. In those with recurrent and prolonged tachycardias, there may be a tendency toward fatigue and reduced exercise tolerance due to decreased ventricular filling during tachycardia phases.
In patients with very frequent episodes, AVNRT may over time induce electrophysiological remodeling of the AV node, making tachycardia easier to trigger and increasing the likelihood of future episodes. In such cases, a careful cardiological evaluation is required to determine the need for definitive treatment.
The diagnosis of atrioventricular nodal reentrant tachycardia (AVNRT) is based on clinical assessment and electrocardiographic confirmation of the arrhythmia. Diagnostic suspicion arises from the presence of regular tachycardia with abrupt onset and termination, typically between 140 and 250 bpm. Patients often report sudden palpitations, sometimes associated with dyspnea or dizziness, and may describe a clear trigger such as stress, physical exertion, or postural changes.
During an AVNRT attack, physical examination reveals regular tachycardia with a rapid, easily palpable pulse. Blood pressure is generally stable, though some patients may develop mild hypotension, especially in prolonged tachycardia. In those with very frequent episodes, pronounced jugular a waves may be observed, due to atrial contraction against a closed tricuspid valve.
The 12-lead electrocardiogram (ECG) is the main diagnostic tool and distinguishes AVNRT from other supraventricular tachycardias. During an episode, the ECG shows the following features:
The most common form, typical AVNRT (slow-fast), is characterized by non-visible P waves embedded in the QRS, while in atypical AVNRT (fast-slow), P waves are more evident and positioned further from the QRS complex.
In patients with sporadic episodes or those not captured by standard ECG, prolonged monitoring is essential for diagnostic confirmation. Options include:
If the diagnosis remains unclear, pharmacological or physiological tests can be performed to assess AV node involvement. Adenosine is the drug of choice to terminate the arrhythmia and confirm AV node participation in the reentrant circuit. Intravenous administration produces a transient AV block, immediately terminating the tachycardia if it is AVNRT. Alternatively, vagal maneuvers such as carotid sinus massage or the Valsalva maneuver can slow AV conduction and unmask retrograde P waves.
In patients with recurrent and disabling episodes, or when the diagnosis remains uncertain despite monitoring, electrophysiological study (EPS) is the most accurate method to confirm the presence of a reentrant AV nodal circuit. This examination allows:
For ablation candidates, EPS allows precise mapping of the reentrant circuit and guides definitive therapy, increasing the probability of success.
The management of atrioventricular nodal reentrant tachycardia (AVNRT) has three main goals: termination of the acute episode, prevention of recurrences, and, in the most severe or frequent cases, definitive therapy with catheter ablation. The choice of strategy depends on symptom severity, episode frequency, and response to pharmacological or non-pharmacological treatments.
In patients experiencing an acute AVNRT episode, the first-line therapy is vagal maneuvers, which increase parasympathetic tone and slow AV nodal conduction. The Valsalva maneuver and carotid sinus massage are the most widely used. If vagal maneuvers are ineffective, intravenous adenosine is administered, producing transient AV block and interrupting the reentry circuit in most cases.
If adenosine is contraindicated or ineffective, beta-blockers or non-dihydropyridine calcium channel blockers (verapamil and diltiazem) can be used to reduce AV conduction and facilitate tachycardia termination. Electrical cardioversion is rarely necessary and is reserved for hemodynamically unstable or pharmacologically refractory patients.
In patients with sporadic, well-tolerated episodes, the main strategy is to avoid triggers and monitor disease progression. However, in those with frequent or symptomatic tachycardias, maintenance pharmacotherapy may be needed. The most commonly used drugs for preventing episodes are beta-blockers and non-dihydropyridine calcium channel blockers, which reduce AV conduction and decrease the likelihood of tachycardia initiation.
For patients who do not respond adequately to beta-blockers or calcium channel blockers, class IC antiarrhythmic agents such as flecainide and propafenone may be considered. However, these drugs should be avoided in those with structural heart disease due to the risk of proarrhythmic effects.
In patients with frequent episodes, disabling symptoms, or poor response to drugs, radiofrequency catheter ablation is the treatment of choice. This procedure is performed during electrophysiological study and involves selective ablation of the AV nodal slow pathway, eliminating the substrate for reentry circuit formation.
Ablation of AVNRT has a success rate above 95% and a low risk of recurrence. Complications are rare and include possible injury to the fast pathway, requiring pacemaker implantation in less than 1% of cases.
The prognosis of AVNRT is generally favorable, especially in patients without structural heart disease. In those who respond well to vagal maneuvers or drugs, episodes can be managed effectively without the need for further intervention. However, in patients with very frequent or highly symptomatic episodes, quality of life may be impaired, necessitating definitive ablation therapy.
In patients treated with catheter ablation, the likelihood of complete arrhythmia resolution is very high, and most no longer require antiarrhythmic therapy. The risk of recurrence is low and occurs mainly in the first months after the procedure, while the risk of long-term complications is extremely low.
In patients with very frequent, untreated tachycardias, there is a risk of tachycardiomyopathy, a condition in which sustained elevated heart rate leads to reversible ventricular dysfunction. For this reason, in patients with recurrent episodes, timely evaluation is recommended to define the most appropriate therapeutic strategy.
Atrioventricular nodal reentrant tachycardia (AVNRT) is generally a benign arrhythmia, but in cases of very frequent or prolonged episodes, certain complications may occur, affecting patient quality of life and, in rare cases, cardiac function.
In patients with particularly frequent and sustained AVNRT episodes, persistent elevated heart rate can lead to left ventricular overload and progressive contractile dysfunction. This condition, known as tachycardiomyopathy, is potentially reversible with arrhythmia control, but in advanced cases may require specific management to restore myocardial function.
In subjects with reduced cardiac reserve, episodes of prolonged tachycardia may reduce ventricular filling and cause hypotension, with possible syncope or presyncope. This risk is higher in patients with underlying heart disease, where tachycardia can further compromise diastolic and systolic function.
Although AVNRT is generally stable over time, in some patients progression to other forms of supraventricular tachycardia, particularly atrial fibrillation, may occur. This phenomenon is more frequent in those with arrhythmic predisposition or atrial structural changes, where electrical remodeling may promote the development of more complex arrhythmic circuits.
Catheter ablation is a safe and effective treatment with a low risk of complications. However, in a small percentage of patients, injury to the fast pathway may occur during slow pathway ablation, resulting in complete atrioventricular block and the need for permanent pacemaker implantation. This event is rare, with an incidence below 1%, but represents the main complication of the procedure.