Atrial supraventricular tachycardia. Supraventricular Tachycardia: Symptoms, Causes, and Treatment Options

03.08.202308.07.2023 by alexxlab

What are the symptoms of supraventricular tachycardia. How is supraventricular tachycardia diagnosed. What treatment options are available for supraventricular tachycardia. Who is at risk for developing supraventricular tachycardia. How can supraventricular tachycardia be prevented.

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Understanding Supraventricular Tachycardia: An Overview

Supraventricular tachycardia (SVT) is a cardiac dysrhythmia characterized by an abnormally fast heart rate originating at or above the atrioventricular (AV) node. This condition is defined by a narrow QRS complex (less than 120 milliseconds) and a heart rate exceeding 100 beats per minute (bpm). A specific type of SVT, known as atrioventricular nodal reentrant tachycardia (AVNRT) or paroxysmal SVT, typically presents with a ventricular rhythm of around 160 bpm and occurs intermittently without apparent triggers.

SVT can significantly impact a person’s quality of life and, in some cases, lead to serious complications. Understanding its causes, symptoms, and treatment options is crucial for both healthcare providers and patients.

Pathophysiology of Supraventricular Tachycardia

To comprehend SVT, it’s essential to understand the heart’s electrical conduction system. The normal electrical pathway begins at the sinoatrial (SA) node, travels through the atrial tissue to the atrioventricular (AV) node, where it experiences a brief delay, and then continues through the His-Purkinje system to the ventricles.

What causes SVT? The most common mechanism is an orthodromic reentry phenomenon. In this scenario, electrical conduction follows the normal path from the atria to the AV node and ventricles, but then travels back to the atria through an accessory pathway. This creates a circular electrical pattern that can sustain the tachycardia.

Types of Supraventricular Tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT)
Atrial tachycardia
Junctional tachycardia
Atrial fibrillation
Atrial flutter
Multi-atrial tachycardia

Each type of SVT has its unique characteristics and may require different approaches to diagnosis and treatment.

Epidemiology and Risk Factors for Supraventricular Tachycardia

SVT is a relatively common cardiac arrhythmia, with AVNRT having an incidence of 35 per 10,000 person-years or 2.29 per 1000 persons. It is the most prevalent non-sinus tachydysrhythmia in young adults.

Who is most at risk for developing SVT? Several factors influence the likelihood of experiencing this condition:

Gender: Women have twice the risk of developing paroxysmal SVT compared to men.
Age: Older individuals have a five times higher risk compared to younger people.
Pediatric population: SVT is the most common symptomatic dysrhythmia in infants and children.
Congenital heart disease: Children with this condition are at increased risk for SVT.
Age-specific etiology: In children under 12, an accessory atrioventricular pathway causing reentry tachycardia is the most common cause of SVT.

Understanding these risk factors can help healthcare providers identify individuals who may be more susceptible to SVT and implement appropriate preventive measures or early interventions.

Recognizing the Symptoms of Supraventricular Tachycardia

SVT can manifest in various ways, and the severity of symptoms can differ from person to person. What are the common symptoms of SVT? Patients typically present with:

Anxiety
Palpitations
Chest discomfort
Lightheadedness
Syncope (fainting)
Dyspnea (shortness of breath)

In more severe cases, patients may experience:

Shock
Hypotension
Signs of heart failure
Exercise intolerance

It’s important to note that some individuals may be asymptomatic, with the tachycardia discovered during routine screening, such as at pharmacies or through fitness trackers. The onset of SVT is typically abrupt and can be triggered by physical activity or emotional stress.

Diagnosis and Evaluation of Supraventricular Tachycardia

Accurate diagnosis of SVT is crucial for appropriate management. How is SVT diagnosed? The primary diagnostic tool is an electrocardiogram (ECG). What are the characteristic ECG findings in SVT?

Narrow QRS complex (<120 milliseconds)
Regular tachycardia with a rate of approximately 180 to 220 beats per minute
Absence of detectable P waves in most cases

If P waves are visible, healthcare providers should consider other diagnoses such as sinus tachycardia or atrial fibrillation. The physical examination, aside from tachycardia, is typically normal in patients with good cardiovascular reserve. However, those beginning to decompensate may show signs of congestive heart failure, such as bibasilar crackles, a third heart sound (S3), or jugular venous distention.

Additional Diagnostic Procedures

While an ECG is the primary diagnostic tool, additional tests may be necessary to confirm the diagnosis or rule out other conditions. These may include:

Holter monitor: A portable ECG device worn for 24-48 hours to capture intermittent episodes of SVT
Event recorder: A wearable device that can be activated by the patient during symptomatic episodes
Echocardiogram: To assess heart structure and function
Electrophysiology study: An invasive test to map the heart’s electrical system and identify the exact location and mechanism of the arrhythmia

Treatment Approaches for Supraventricular Tachycardia

The management of SVT depends on the severity of symptoms, frequency of episodes, and underlying causes. What are the main treatment options for SVT?

Acute Management

For acute episodes of SVT, the following interventions may be employed:

Vagal maneuvers: Techniques such as the Valsalva maneuver or carotid sinus massage can stimulate the vagus nerve and potentially terminate the arrhythmia
Medications: Adenosine is often the first-line pharmacological treatment for acute SVT
Cardioversion: In cases where medications are ineffective or contraindicated, electrical cardioversion may be necessary

Long-term Management

For patients with recurrent SVT, long-term management strategies include:

Antiarrhythmic medications: Beta-blockers, calcium channel blockers, or other antiarrhythmic drugs may be prescribed to prevent recurrences
Catheter ablation: A minimally invasive procedure to eliminate the abnormal electrical pathway causing SVT
Lifestyle modifications: Avoiding triggers such as caffeine, alcohol, and stress can help reduce episodes

The choice of treatment depends on individual factors, including the patient’s age, overall health, and preferences. A personalized approach is essential for optimal management of SVT.

Prevention and Lifestyle Considerations for Supraventricular Tachycardia

While not all cases of SVT can be prevented, certain lifestyle modifications can help reduce the frequency and severity of episodes. How can individuals minimize their risk of SVT?

Manage stress: Practice relaxation techniques such as meditation or yoga
Avoid triggers: Limit consumption of caffeine, alcohol, and nicotine
Maintain a healthy weight: Obesity can increase the risk of SVT
Regular exercise: Engage in moderate physical activity, as recommended by a healthcare provider
Adequate sleep: Ensure sufficient and quality sleep to reduce stress on the body
Stay hydrated: Proper hydration can help maintain electrolyte balance

It’s important to note that these preventive measures may not be effective for all individuals with SVT, and medical management may still be necessary.

The Role of Interprofessional Care in Managing Supraventricular Tachycardia

Effective management of SVT often requires a collaborative approach involving various healthcare professionals. Why is interprofessional care important in SVT management?

Comprehensive assessment: Different specialists can provide insights into various aspects of the condition
Tailored treatment plans: A team approach allows for personalized care based on the patient’s specific needs
Improved patient education: Multiple professionals can reinforce important information and self-management strategies
Continuity of care: Coordination among team members ensures consistent and ongoing management

An interprofessional team for SVT management may include:

Cardiologists
Electrophysiologists
Primary care physicians
Nurses specializing in cardiac care
Pharmacists
Nutritionists
Mental health professionals

By working together, these professionals can provide comprehensive care that addresses all aspects of SVT, from acute management to long-term prevention and lifestyle modifications.

Future Directions in Supraventricular Tachycardia Research and Treatment

As our understanding of SVT continues to evolve, new avenues for research and treatment are emerging. What are some promising areas of investigation in SVT management?

Advanced mapping technologies: Improved methods for identifying and localizing arrhythmia sources
Novel ablation techniques: More precise and less invasive approaches to eliminate abnormal electrical pathways
Genetic studies: Investigating genetic factors that may predispose individuals to SVT
Personalized medicine: Tailoring treatments based on individual genetic and physiological profiles
Wearable technology: Developing more sophisticated devices for continuous monitoring and early detection of SVT episodes

These advancements hold the potential to improve diagnosis, treatment efficacy, and quality of life for individuals affected by SVT. Ongoing research in these areas may lead to more targeted and effective interventions in the future.

In conclusion, supraventricular tachycardia is a complex cardiac condition that requires a multifaceted approach to diagnosis, treatment, and management. By understanding its pathophysiology, recognizing symptoms, and implementing appropriate interventions, healthcare providers can significantly improve outcomes for patients with SVT. Continued research and interprofessional collaboration will be key to advancing our ability to manage this condition effectively and enhance the quality of life for those affected by SVT.

Supraventricular Tachycardia – StatPearls – NCBI Bookshelf

Continuing Education Activity

Supraventricular tachycardia (SVT) is a dysrhythmia originating at or above the atrioventricular (AV) node and is defined by a narrow complex (QRS < 120 milliseconds) at a rate > 100 beats per minute (bpm). Atrioventricular nodal reentrant tachycardia (AVNRT), also known as paroxysmal SVT, is defined as intermittent SVT without provoking factors, and typically presents with a ventricular rhythm of 160 bpm. This activity describes the cause, pathophysiology, and presentation of SVT and stresses the importance of an interprofessional team in its management.

Objectives:

Describe the pathophysiology of SVT.
Outline the presentation of a patient with SVT.
Summarize the treatment options for SVT.
Review the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by SVT.

Access free multiple choice questions on this topic.

Introduction

Atrioventricular nodal reentrant tachycardia (AVNRT), also known as paroxysmal SVT, is defined as intermittent SVT without provoking factors, and typically presents with a ventricular rhythm of 160 bpm. [1][2][3]

Etiology

The differential diagnosis includes sinus tachycardia, atrial tachycardia, junctional tachycardia, atrial fibrillation, atrial flutter, or multi atrial tachycardia.

In patients susceptible to SVT, medications, caffeine, alcohol, physical or emotional stress, or cigarette smoking can trigger SVT.[4][5]

Epidemiology

The incidence of atrioventricular nodal reentrant tachycardia is 35 per 10,000 person-years or 2.29 per 1000 persons and is the most common non-sinus tachydysrhythmia in young adults. Women have two times higher risk of developing paroxysmal SVT in comparison to men, and older individuals have five times higher compared to a younger person.

SVT is the most common symptomatic dysrhythmia in infants in children. Children with congenital heart disease are it increased risk for SVT. In children younger than 12 years old, an accessory atrioventricular pathway causing reentry tachycardia is the most common cause of SVT. [6][7]

Pathophysiology

The electrical conduction through the heart starts at the sinoatrial (SA), which then travels to the surrounding atrial tissue to the atrioventricular (AV) node. At the AV node, the electrical signal is delayed for approximately 100 milliseconds. Once through the AV node, the electrical signal travels through the His-Purkinje system, which distributes the electrical signal to the left and right bundles, and ultimately to the myocardium of the ventricles. The pause at the AV node allows the atria to contract and empty before ventricular contraction.

The most common cause of SVT is an orthodromic reentry phenomenon, which occurs when the tachycardia is secondary to normal anterograde electrical conduction from the atria to the AV node to the ventricles, with retrograde conduction via an accessory pathway from the ventricles back to the atrial.

A narrow QRS complex (< 120 milliseconds) indicates the ventricles are being activated superior to the His bundle via the usual pathway through the His-Purkinje system. This implies that the arrhythmia originates from the sinoatrial (SA) node, the atrial myometrium, the AV node, or within the His bundle.

In the rarer antidromic conduction, conduction passes from the atria to the ventricles via the accessory pathway, then returns retrograde through the AV node to the atria. [8]

History and Physical

Patients typically present with anxiety, palpitations, chest discomfort, lightheadedness, syncope, or dyspnea. In some cases, a patient may present with shock, hypotension, signs of heart failure, lightheadedness, or exercise intolerance. Some may present without symptoms, and the tachycardia is discovered during routine screening, for example, at pharmacies or with fitness trackers. The onset is typically abrupt and can be triggered by stress secondary to physical activity or emotional stress.

Physical exam, aside from tachycardia, is typically normal in a patient with good cardiovascular reserve. Patients beginning to decompensated may show signs of congestive heart failure, (bibasilar crackles, a third heart sound (S3), or jugular venous distention).

Evaluation

The first test to evaluate for SVT is to obtain an ECG. [9][10][11]

ECG characteristic includes a narrow complex, regular tachycardia with a rate of approximately 180 to 220 beats per minute. P waves are not detectable. If P waves are detectable, consider sinus tachycardia or atrial fibrillation or flutter as a potential etiology.

The remainder of the evaluation is focused on trying to isolate a cause of SVT, for example, electrolyte abnormalities, anemia, or hyperthyroidism. Consider checking a digoxin level of patients using that drug, as SVT can be secondary to supratherapeutic digoxin concentrations.

Treatment / Management

Once an SVT is identified, the next objective is to assess for hemodynamic instability. Signs of hemodynamic instability include hypotension, hypoxia, shortness of breath, chest pain, shock, evidence of poor end-organ perfusion, or altered mental status.[12][13]

If a patient is unstable, consider immediate synchronized cardioversion. It is important that the defibrillator is placed in a sync mode, typically indicated by a marker on the defibrillator screen noting each QRS complex. This mode allows the defibrillator to deliver the shock synchronized with the QRS complex, to prevent the shock from being delivered during the T-wave, while the heart is depolarized. The R on T phenomenon can cause polymorphic ventricular tachycardia. In adults, the starting dose for synchronized cardioversion is 100 joules to 200 joules and can be increased in a stepwise fashion if unsuccessful at lower doses. In children, the first dose for cardioversion is 0.5 J/kg to 1 J/kg and can be doubled to 2 J/kg on subsequent attempts.

In a stable patient, attempted vagal maneuvers while preparing for chemical cardioversion, including the Valsalva maneuver and carotid massage. Both of these act to stimulate the parasympathetic system. This slows impulse formation at the sinus node, slows conduction velocity at the AV node, lengthens the AV node refractory period, and decreases ventricular inotropy.

The Valsalva maneuver is performed expiring against a closed glottis, and needs to be held for 10 seconds to 15 seconds. Patients can achieve this by bearing down as if they are going to have a bowel movement. Younger children can blow out through a syringe or straw. In infants and toddlers, ice packs applied to the face can cause a similar vagal reaction. Although ocular pressure can cause a vagal reaction, it is not recommended as it can lead to a ruptured globe if excessive force is used.

Carotid massage involves placing the patient in a supine position with the neck extended, and applying pressure to one carotid sinus for approximately 10 seconds. Carotid massage is contraindicated in patients with carotid bruit, or who have had a prior transient ischemic attack or cerebral vascular accident in the last three months. Carotid massage is not indicated in children or infants.

The REVERT trial demonstrated that a modified Valsalva maneuver, with the traditional Valsalva maneuver being held for 60 seconds at a 45 degree recumbent position, then being switched to a recumbent position with the legs held at 45 degrees angle for 15 seconds, was more efficacious than the standard Valsalva maneuver. [14]

If vagal maneuvers are ineffective, treat with adenosine. Adenosine is rapidly metabolized in the periphery, and therefore must be given as a rapid push through a large, ideally peripheral, intravenous route. The initial dose is 6 mg intravenously (IV) (pediatric dose 0.1 mg/kg, maximum dose 6 mg). If the initial dose is ineffective, adenosine may be dosed again at 12 mg IVP (pediatric dose 0.2 mg/kg, maximum dose 12 mg). The second dose of adenosine 12 mg IVP may be repeated one additional time if there is no effect. Each dose of adenosine needs to be flushed rapidly with 10 mL to 20 mL normal saline. Often two person administration, with one person administering the adenosine at a proximal IV port, and a second person flushing the IV line via a distal port immediately after adenosine administration, is required to adequate flush in the adenosine.

Consider reducing the adenosine dose to 3 mg IVP if the patient is currently receiving carbamazepine or dipyridamole, is the recipient of a heart transplant, or adenosine is being given through a central line.

In the event of a patient with a misinterpreted rhythm, the administration of adenosine can help slow down the heart rate long enough to determine if the cause of the patient’s tachycardia is due to a different narrow complex tachycardia (e.g., atrial fibrillation or atrial flutter).

If adenosine fails, second line medications include diltiazem (0.25 mg/kg IV loading dose followed by 5mg/hr to 15 mg/hr infusion), esmolol (0.5 mg/kg IV loading dose, then 0. 5 mg/kg/min up to 0.2 mg/kg/min, will need to repeat bolus for every up-titration), or metoprolol (2.5 mg to 5 mg IV every two to five minutes, not to exceed 15 mg over 10 to 15 minutes).

These measures still prove ineffective, overdrive pacing, or pacing the heart at a faster rate than its native rhythm, can help discontinue SVT. However, there is an increased risk of ventricular tachycardia or fibrillation, and therefore should be used with caution and with cardioversion immediately available.

Patients with recurrent SVT without a pre-excitation syndrome may require long-term maintenance with oral beta-blockers or calcium to maintain sinus rhythm. They may also require radio-frequency ablation if an accessory pathway is identifiable. Patients should be counseled on how to perform vagal maneuvers on their own for long-term management of recurrent SVT. [2][15]

Differential Diagnosis

Complications

Complications are either related to the medications or radiofrequency ablation. Since the latter is an invasive procedure the following complications may occur:

Hematoma
Pseudoaneurysm of the artery
Bleeding
Myocardial infarction
Heart block and the need for a pacemaker
Stroke
Death

Pearls and Other Issues

Wolff-Parkinson-White (WPW) syndrome is an example of an accessory pathway syndrome, characterized by a short PR interval (< 120 ms), a prolonged QRS (> 100 ms), and a delta wave (a slurred upstroke to the QRS complex). Patients with WPW can occasionally present with an antidromic reentry tachycardia, in which the accessory pathway is the anterograde limb, and the AV node is the retrograde pathway. These typically present with a wide complex, regular, and extremely rapid tachycardia. In these cases, AV nodal blocking agents like adenosine are contraindicated because they can allow unopposed retrograde conduction through the accessory pathway, leading to ventricular tachycardia or fibrillation. Procainamide (15 mg/kg to 18 mg/kg loading dose, 1 mg/min to 4 mg/min maintenance infusion) is the first-line treatment of this tachydysrhythmia, followed by amiodarone (150 mg over 10 minutes, followed by 360 mg over six hours, then 540 mg over 18 hrs). For ventricular rates greater than 250 bpm, consider synchronized cardioversion at 100 J to 200 J.

Enhancing Healthcare Team Outcomes

Paroxysmal SVT is usually managed by an interprofessional team of healthcare workers dedicated to cardiac arrhythmias. Since these arrhythmias cannot be prevented, the focus is on treatment. Besides the cardiologist, the role of the nurse and pharmacist is indispensable. The patient should be educated about this arrhythmia and the potential risk of sudden death if left untreated. For patients with SVT managed with medications, the pharmacist should assist the team by educating the patient on potential adverse effects, drug interactions and the need for close follow-up. The patient should also be educated on the option of radiofrequency ablation, which has a much higher success rate compared to medications. [16](Level II)

Outcomes

For the most part, patients with paroxysmal SVT have a good outcome with treatment. However, a small number of patients with WPW do have a tiny risk of sudden death. In patients with SVT arising due to a structural defect in the heart, the prognosis depends on the severity of the defect, but in healthy people with no structural defects, the prognosis is excellent. Pregnant women who develop SVT do have a slightly higher risk of death if there is an unrepaired heart defect. [17][18][19](Level V)

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Figure

Lead II (2) Supraventricular tachycardia SVT. Contributed by Wikimedia Commons, James Heilman, MD (Public Domain-Self)

Figure

A graphical representation of the Electrical conduction system of the heart showing the Sinoatrial node, Atrioventricular node, Bundle of His, Purkinje fibers, and Bachmann’s bundle. Contributed by Wikimedia Commons (Public Domain)

Figure

This is a recording of the termination of a supraventricular tachycardia at about 130/min. which terminates and leaves a pause and then sinus bradycardia. This is a from of “tachy/brady” syndrome where a tachycardia is followed by a bradycardia. Contributed (more…)

References

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: Disclosure: Laryssa Patti declares no relevant financial relationships with ineligible companies.
: Disclosure: John Ashurst declares no relevant financial relationships with ineligible companies.