AV nodal reentrant tachycardia: Difference between revisions
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*Some patients will develop [[syncope]] during episodes of AVRNT. Those patients who do become symptomatic during episodes of AVNRT (i.e. have [[syncope]]) should avoid activities where the occurrence of [[hemodynamic compromise]] would endanger their safety or that of others (like driving). | *Some patients will develop [[syncope]] during episodes of AVRNT. Those patients who do become symptomatic during episodes of AVNRT (i.e. have [[syncope]]) should avoid activities where the occurrence of [[hemodynamic compromise]] would endanger their safety or that of others (like driving). | ||
*In patients with underlying [[ischemic heart disease]], demand-related [[myocardial ischemia]], [[angina]] and even [[myocardial infarction]] and/or [[congestive heart failure]] can occur. | *In patients with underlying [[ischemic heart disease]], demand-related [[myocardial ischemia]], [[angina]] and even [[myocardial infarction]] and/or [[congestive heart failure]] can occur. | ||
*Tachycardia mediated cardiomyopathy | *[[Tachycardia mediated cardiomyopathy]] | ||
===Prognosis=== | ===Prognosis=== | ||
Revision as of 16:16, 5 September 2012
| AV nodal reentrant tachycardia | |
 | |
|---|---|
| AV nodal reentrant tachycardia. In yellow, is evidenced the P wave that falls after the QRS complex. | |
| ICD-10 | I47.1 |
| ICD-9 | 426.89, 427.0 |
| MeSH | D013611 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Synonyms and keywords: AVNRT; AV node reentrant tachycardia; AV nodal reentry tachycardia; AV node reentry tachycardia; atrioventricular node reentrant tachycardia; atrioventricular nodal reentry tachycardia; atrioventricular node reentry tachycardia;
Overview
AV nodal reentrant tachycardia is a type of tachycardia (fast rhythm) of the heart. It is one of several types of supraventricular tachycardia (SVT), and like all SVTs the electrical impulse originates proximal to the bundle of HIS. In the case of AVNRT, the electrical impulse originates in the AV node and the immediately surrounding tissue. AVNRT is the most common cause of supraventricular tachycardia.
Historical Perspective
In the past, many cases of AVNRT were referred to as paroxysmal atrial tachycardia, or PAT, or PAT with block. With greater understanding of the underlying electrophysiologic mechanism of these arrhythmias, more specific terminology has now been adapted, and these older non-specific terms are now used to refer to supraventricular tachycardia in general rather than AVNRT in specific.
Pathophysiology
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferiorly and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. In the usual form of AVNRT, the conduction from the atrium to the ventricle is down the slow pathway, and the retrograde conduction from the ventricle to the atrium is up the fast pathway.
Electrophysiologic Triggers
Premature Atrial Complex
The most common trigger for an episode of AVNRT is when an atrial premature complex (APC) approaches the fast pathway, and is blocked due to the longer refractory period of this pathway, and instead conducts down the slow pathway. As the impulse goes down the slow pathway, the fast pathway recovers, and allows the impulse to conduct backward or retrograde toward the atrium. It then re-enters the atrial entrance of the slow pathway and the cycle repeats itself.
Premature Ventricular Complex
The second most common mechanism whereby AVNRT is triggered is via the entry of a premature ventricular complex down either the slow conducting pathway (similar to a premature atrial complex above) or down the rapidly conducting pathway.
Classification
There are several types of AVNRT. The "common form" or "usual" AVNRT utilizes the slow AV nodal pathway as the anterograde limb of the circuit and the fast AV nodal pathway as the retrograde limb. The reentry circuit can be reversed such that the fast AV nodal pathway is the anterograde limb and the slow AV nodal pathway is the retrograde limb. This, not surprisingly is referred to as the "uncommon form" of AVNRT. However, there is also a third type of AVNRT that utilizes the slow AV nodal pathway as the anterograde limb and left atrial fibers that approach the AV node from the left side of the inter-atrial septum as the retrograde limb. This is known as atypical, or Slow-Slow AVNRT.
Common AVNRT
In common AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction is via the fast pathway ("slow-fast" AVNRT).
Because the retrograde conduction is via the fast pathway, stimulation of the atria (which produces the inverted P wave) will occur at the same time as stimulation of the ventricles (which causes the QRS complex). As a result, the inverted P waves may not be seen on the surface ECG since they are buried with the QRS complexes. Often the retrograde p-wave is visible, but also in continuity with the QRS complex, appearing as a "pseudo R prime" wave in lead V1 or a "pseudo S" wave in the inferior leads.
Uncommon AVNRT
In uncommon AVNRT, the anterograde conduction is via the fast pathway and the retrograde conduction is via the slow pathway ("fast-slow" AVNRT). Multiple slow pathways can exist so that both anterograde and retrograde conduction are over slow pathways. ("slow-slow" AVNRT).
Because the retrograde conduction is via the slow pathway, stimulation of the atria will be delayed by the slow conduction tissue and will typically produce an inverted P wave that falls after the QRS complex on the surface ECG.
Detailed Chapters on AVNRT Variants
Risk Factors
Underlying structural heart disease is generally absent. Often, there is no precipitant of an episode. Risk factors for precipitation of AVNRT include:
- Alcohol
- Caffeine
- Hyperthyroidism
- Hypokalemia
- Hypomagnesemia
- Myocardial ischemia
- Psychological stress
Differentiating AVNRT from other Disorders
The fast and slow pathways of AVNRT should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW) syndrome or atrioventricular re-entrant tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium in close proximity to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings, they provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium. AVNRT must be distinguished from other tachycardias such as atrial fibrillation, atrial flutter, sinus tachycardia, ventricular tachycardia and tachyarrhythmias related to Wolff-Parkinson-White syndrome, all of which may have symptoms that are similar to AVNRT.
Epidemiology and Demographics
AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia and accounts for 60% to 70% of these cases.
Sex
The ratio of female to male involvement is 3:1
Age
There is no age predilection.
Natural History, Complications, Prognosis
Complications
- Some patients will develop syncope during episodes of AVRNT. Those patients who do become symptomatic during episodes of AVNRT (i.e. have syncope) should avoid activities where the occurrence of hemodynamic compromise would endanger their safety or that of others (like driving).
- In patients with underlying ischemic heart disease, demand-related myocardial ischemia, angina and even myocardial infarction and/or congestive heart failure can occur.
- Tachycardia mediated cardiomyopathy
Prognosis
AVNRT is rarely life threatening and in the absence of underlying structural heart disease, the prognosis is good. Radiofrequency ablation is curative in 95% of cases.
Diagnosis
Symptoms
The following symptoms may be present:
- Sudden onset and sudden offset of rapid palpitations is common
- Dizziness and rarely syncope, especially at the onset of the episode of tachycardia
- Chest pain and angina if the patient has ischemic heart disease
Laboratory Studies
Depending upon the patient's history and demographics, the following laboratory studies should be considered:
- Thyroid function tests (TFTs) - an overactive thyroid may increase the risk of AVNRT
- Electrolytes - hypokalemia, hypomagnesemia may predispose to AVNRT
- Cardiac markers - if there is a concern that myocardial infarction (a heart attack) has occurred either as a cause or as a result of the AVNRT; this is usually only the case if the patient has experienced ischemic chest pain
Electrocardiogram
An electrocardiogram performed during the occurrence of symptoms may confirm the diagnosis of AVNRT.
Holter Monitor / Event Recorder
If the patient complains of recurrent palpitations and no arrhythmia is present on the resting EKG, then a Holter Monitor or Cardiac Event Monitor should be considered.
Treatment
An episode of supraventricular tachycardia (SVT) due to AVNRT can be terminated by any action that transiently blocks the AV node. Various methods are possible.
Vagal maneuvers
Some people with known AVNRT may be able to stop their attack by using various tricks to activate the vagus nerve. This includes carotid sinus massage (pressure on the carotid sinus in the neck) or the Valsalva maneuver (increasing the pressure in the chest by attempting to exhale against a closed airway).
Medication
Medical therapy can be initiated with AV nodal slowing drugs such as adenosine (which is a pharmacologic cardioversion), beta blockers or non-dihydropyridine calcium channel blockers (such as verapamil). Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma.
Cardioversion
In very rare instances, cardioversion (the electrical restoration of a normal heart rhythm) is needed in the treatment of AVNRT. This would normally only happen if all other treatments have been ineffective, or if the fast heart rate is poorly tolerated (e.g. the development of heart failure symptoms, low blood pressure or coma).
Electrophysiology
After being diagnosed with AVNRT, patients can also undergo an electrophysiology (EP) study to confirm the diagnosis. Catheter ablation of the slow pathway, if successfully carried out, can potentially cure the patient of AVNRT.