Continuing Education Activity
Reentrant arrhythmias are a diverse group of cardiac conduction defects that can manifest in a wide range of presentations. Proper diagnosis is crucial in the management of this condition. This condition has low mortality but if managed incorrectly can result in sudden cardiac death. This activity describes the treatment, management, and diagnosis of patients with reentrant arrhythmias and highlights the role of the interprofessional team in caring for affected patients.
- Outline the stepwise approach for the evaluation of reentrant arrhythmias.
- Summarize treatment modalities available for a patient with a reentrant arrhythmia.
- Review the pathophysiology of various reentrant arrhythmias and how to differentiate between them on patient presentation.
- Describe how the coordination of an interprofessional team can lead to a more rapid diagnosis of reentrant arrhythmias and subsequently decrease associated morbidity and mortality in affected patients.
Reentrant arrhythmias are distinct electrophysiology maladies of the heart caused by the presence of circuits in the normal myocardium. Atrioventricular nodal reentry tachycardia (AVNRT), the most common reentrant supraventricular tachycardia (SVT), utilizes the AV node as its circuit. Other reentrant tachycardias such as Wolff-Parkinson White (WPW) syndrome, utilizes an accessory pathway to create the reentrant circuit.
Reentry occurs when the propagating electrophysiological signal fails to succumb to its normal continuance and persists, re-exciting the heart after the refractory period. This constant re-excitation of the heart can produce a heart rate of over 250 beats per minute. However, the typical range is usually 180 to 200 beats per minute in adults. Occasionally, hypotension can occur with prolonged episodes at a rapid ventricular rate.
Reentry arrhythmias can manifest in a multitude of ways depending on the specific variation of the abnormal rhythm. If the origin involves the atrioventricular (AV) node, the arrhythmia purely occurs due to an anatomic abnormality in the AV node associated with the different conduction pathways in the node itself. The AV node has a slow and a fast pathway, which, when operating correctly, does not allow for the re-excitation of the node.
Other reentrant arrhythmias, not involving the AV node, often rise due to anatomic variants within the myocardium. Accessory pathways, pathognomic in Wolff-Parkinson-White (WPW) syndrome, can be iatrogenic from previous cardiac procedures or genetic. This new route, that can be created in a multitude of ways, forms the circuit with the existing, normal, electrophysiological pathways. Genetic origins for non-AV nodal circuits are commonly seen in younger patients with reentrant arrhythmias. Glycogen-storage diseases, mutations of adenosine monophosphate-activated protein kinase, and lysosomal membrane protein mutations have been associated with the formation of the reentrant circuits. Patients with Ebstein anomaly have also been shown to develop accessory pathways, which could lead to the formation of these abnormal circuits causing reentrant arrhythmias.
Arrhythmias with pre-excitation origins are estimated to occur in 1 to 3 per 1000 people in the United States, and 60% to 70% of patients discovered to have evidence of pre-excitation, generally detected on routine electrocardiograms, have no other heart disease. WPW has an incidence of 15 cases per 10,000 patients. WPW is more prevalent in males than in females. The most common location of the accessory pathway in WPW is the left free wall (53%). Other locations where the accessory pathway is seen include the posteroseptal wall (36%), right free wall (8%), and the anteroseptal wall (3%). AVNRT is the most common paroxysmal supraventricular tachycardia. Approximately 89,000 new cases of SVT are discovered each year, with roughly half a million people in the United States currently living with SVTs.
The pathophysiology of reentrant tachycardia depends on the origin and location of the reentrant circuit. A similarity that all reentrant arrhythmias possess is the formation of a circuit that allows for constant re-excitation of the myocardium. This constant re-excitation of the myocardium can manifest in dangerous arrhythmias, syncope, or even sudden death.
If the reentrant circuit is formed within a node, as in with AVNRT, an error in the refractory period with the individual pathways is the source. The AV node has different conduction pathways, each with their own unique physiology aimed to regulate one action potential to create one well-coordinated heartbeat. This is accomplished by two pathways, the slow pathway and the fast pathway, each depolarizing and entering their respective refractory periods at the appropriate time. When a pathway is in its refractory period, no action potentials can pass through. In reentrant arrhythmias occurring in the AV node, this synchronization of depolarization and the refractory period is impaired, allowing the conduction pathways to be re-excited and depolarize again in a retrograde fashion. This creates a constant re-excitation of the atria and ventricles, generating the arrhythmia seen clinically or on an electrocardiogram (EKG).
If the circuit is not nodal in origin, the pathophysiology is much different. In these variants of reentrant arrhythmias, an abnormal conduction pathway exists. This abnormal connection generally isn't regulated by the nodes in the normal conduction pathway, which is necessary for a well-coordinated heartbeat. In WPW, an accessory pathway exists between the atria and the ventricles. The abnormal connection does not have to go through the AV node; thus, it can depolarize the ventricles earlier than in sinus rhythm, represented by the sloping delta wave seen on WPW EKGs. Since there is an unregulated conduction pathway, the reentrant circuit can form when a connection is made with the abnormal pathway and the normal conduction pathway.
History and Physical
Patients who are diagnosed with reentrant arrhythmias have a multitude of presentations. Patients commonly present with palpitations or chest pain but can also be entirely asymptomatic. If asymptomatic, the diagnosis is likely found on a routine EKG or a rhythm strip while being worked up for another complaint. Other symptoms commonly seen in patients with reentrant arrhythmias are nervousness, anxiety, neck pounding, lightheadedness, and even syncopal episodes.
An accurate past medical and surgical history is paramount when working up a patient with suspected reentrant arrhythmia. Since these arrhythmias can be iatrogenic, any cardiac surgery would be an important history to gather from the patient. One should also derive information on medications, illicit drug use, and past medical history that need to be obtained in order to consider other differentials.
In symptomatic patients, the first thing that needs to be evaluated is the patient’s hemodynamic stability. A proper physical exam is required to work up possible differentials and rule out triggering conditions that would elicit another condition mimicking signs of this arrhythmia. Many patients who truly have a reentrant arrhythmia will have a completely normal exam. The most common abnormal physical exam findings that present in patients with these conduction deficiencies are tachycardia and irregular heart rhythm. The heart rate in patients with tachycardic reentrant arrhythmias typically is in the 150 to 250 beat/minute range.
The first step in evaluation for a patient with a reentrant arrhythmia is to obtain a 12 lead EKG. This can occur in a patient who is symptomatic or a patient seeking treatment for an unrelated condition that requires a routine EKG. Ideally, the patient would also have a baseline EKG to be able to compare the abnormal one to the normal one. An additional benefit to the discovery of the arrhythmia on the EKG is the other clues the EKG offers. The pattern and morphology of the P waves and QRS complexes can tell an experienced reader where the arrhythmia originates and where the reentrant circuit is. A notable example of this is the delta wave found in WPW. The delta wave is sloping at the beginning of the QRS complex, which occurs due to the ventricles' pre-excitation from the accessory pathway found in WPW.
Once the reentrant arrhythmia is diagnosed, further workup is needed if a permanent resolution is to be pursued. One way to more accurately determine the origin of the arrhythmia is to use electrophysiology mapping. The study is crucial, prior to undergoing an ablation, to treat a patient's arrhythmia.
Treatment / Management
There are various modes of management with a patient with a reentrant arrhythmia. If the patient’s arrhythmia originates in the AV node, it is possible a simple manipulation such as a vagal maneuver, can terminate the arrhythmia and set the patient back into sinus rhythm. A vagal maneuver is unlikely to work in a reentrant circuit formed by an accessory pathway or another malformation of the conduction pathway of the heart. If a malformation of the conduction pathway exists, the conduction signal will be likely to continue going down that pathway thus, a vagal maneuver would be ineffective. The patients also should not receive vagal maneuvers if they are hemodynamically unstable or hypotensive.
Recommended vagal maneuvers are the Valsalva maneuver and carotid artery massage. The Valsalva maneuver is performed by instructing the patient to forcefully exhale against a closed glottis. An alternate technique is performed by exhaling against a closed glottis followed by a passive leg raise at a 45-degree angle. The carotid sinus massage is performed by applying pressure to the carotid sinus, which is located inferior to the angle of the mandible at the level of the thyroid cartilage.
If vagal maneuvers fail or are an inappropriate treatment method, pharmacologic therapy should be attempted before any invasive procedures are attempted. Before a specific pharmacologic therapy is chosen, the specific reentrant arrhythmia needs to be identified. Adenosine is a good treatment option in a patient where the AV node is the origin of arrhythmia; however, it can be catastrophic in a patient with a circuit formed by an accessory pathway. If adenosine is given to a patient with Wolff-Parkinson White syndrome, the AV node will be blocked by the medications. However, the accessory pathway will remain uninhibited, which can lead to ventricular fibrillation and possible cardiac arrest. In conclusion, adenosine is a great treatment modality for patients with AVNRT, but physicians should be cautious in its use with patients who have WPW, making imperative the need for accurate diagnostic measures prior to treatment.
Other pharmacologic treatment such as beta-blockers and calcium channel blockers can be used to terminate the arrhythmia. Calcium channel blockers are contraindicated in tachycardic arrhythmias originating in the ventricles. Antiarrhythmic therapy can also be used to terminate the reentrant circuit. Similar to vagal maneuvers, the effectiveness of these treatments is limited if there are malformations of the conduction pathway. Class 1a and 1c antiarrhythmic drugs have shown effectiveness in slowing the conduction velocity in the accessory pathways by prolonging the refractory period in the action potential.
Calcium channel blockers, beta-blockers, and antiarrhythmic agents, such as quinidine, procainamide, amiodarone, and flecainide, are indicated to treat and terminate arrhythmias in patients with WPW.
In AVNRT, adenosine can be pushed to terminate the arrhythmia. As with WPW, calcium channel blockers, beta-blockers, and antiarrhythmic agents such as quinidine, procainamide, amiodarone, and flecainide, are approved treatment modalities for AVNRT.
A more permanent form of treatment is a cardiac ablation. Once the arrhythmia has been identified by cardiac mapping, the specific location of the arrhythmia can be determined. The ablation procedure eliminates and corrects the arrhythmia by destroying the abnormal conduction pathways with heat. In AVNRT, the cure rate is above 95%, with complications below 1%. In WPW, the success rate is above 90% but has a higher rate of complications at 5% to 10%. Any complication from an ablation procedure could lead to a permanent AV block and a need for a pacemaker.
In the unstable patient with any reentrant arrhythmia, advanced cardiovascular life support (ACLS) protocol should be followed. Once the origin of the patient’s instability is determined to be the arrhythmia, direct-current cardioversion is indicated to stabilize the patient. Intravenous access should also be obtained as soon as possible to administer intravenous medications or sedation if the patient is conscious.
Differential diagnoses for reentrant arrhythmias include other arrhythmias. Most reentrant circuits are located above the ventricles, consequently, other supraventricular tachycardias can be confused with reentrant arrhythmias. A 12 lead EKG should be obtained to differentiate these arrhythmias from one another.
- Sinus tachycardia
- Atrial fibrillation
- Atrial flutter
- Atrial tachycardia
- Torsades de pointes
- Anemic state
The prognosis of reentrant arrhythmias is generally good in the absence of any other structural heart defects. Sudden death and other complications can occur while patients are in the arrhythmia, so it is essential to return the patient to sinus rhythm as quickly as possible. Prolonged arrhythmia can lead to hemodynamic instability and cardiac remodeling worsening the prognosis. If medical therapy does not control the malady, then an ablation should be performed to correct the underlying conduction defects and to return the patient to a stable rhythm. A successful ablation can be curative for specific reentrant arrhythmias leaving these patients with an excellent prognosis.
Complications in reentrant arrhythmias vary depending on the origin and anatomic location of the arrhythmia. As with any uncontrolled heart rate, reentrant arrhythmias that result in a tachycardic rate can lead to cardiac remodeling, hemodynamic compromise, and eventually, heart failure.
If the reentrant circuit is formed due to an accessory pathway, such as in Wolff Parkinson White syndrome, the patient can transition into ventricular tachycardia. This rare but well-known complication occurs when the accessory pathway over-stimulates the ventricles causing the heart to go into a more deadly arrhythmia. The fear of ventricular tachycardia and sudden death is why prompt diagnosis and treatment are crucial for patients with WPW syndrome.
Many complications can occur from cardiac ablation. The most common complication is bleeding from the site of insertion. Mechanical trauma to the heart valves, vessels, or the heart itself, potentially rupturing a chamber wall, are other risks this procedure entails. A more rare but worrisome complication is the iatrogenic creation of another arrhythmia, which potentially could make the patient unstable. If the native conduction system is damaged severely, a pacemaker may need to be placed to manage the new arrhythmia or damage to the conduction system.
Deterrence and Patient Education
Patients should be taught that reentrant arrhythmias are caused by a problem with the heart’s conduction mechanism, which coordinates the beating of the heart. They should be informed of the mechanism of the disease, i.e., that the problem occurs when a circuit is formed, causing the conduction system to re-excite itself continuously, and the typical symptoms that they may experience if they are at risk for the disease or have been treated for it in the past. Typical symptoms to mention include anxiety, lightheadedness, palpitations, and losing consciousness. Patients need to be taught to watch for worrisome symptoms such as more than a brief time period of headaches, palpitations, and presyncope symptoms. They should be advised to seek medical attention promptly, especially those treated with ablation who have a recurrence of symptoms.
Enhancing Healthcare Team Outcomes
In a patient with an unstable arrhythmia, an interprofessional team approach with good communication, and established roles is crucial for optimal patient care. Health care professionals trained and oriented to the hospital’s specific policies are important for any rapid response or code blue situation. One study at a Vancouver General Hospital showed that nurses felt the team performed better after training and with assigned team roles. Prior to training, many nurses noted that it was unclear who the team leader was and who had which roles. Establishing proper roles for healthcare professionals is extremely important in unstable patients with an advanced condition such as a reentrant arrhythmia.