Supraventricular tachycardia definition: Supraventricular tachycardia – Symptoms and causes

27.09.198010.12.2021 by alexxlab

Содержание

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

Atrial flutter
Atrial tachycardia
Atrial fibrillation
Ventricular tachycardia

Complications

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

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)

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

1.: Karmegeraj B, Namdeo S, Sudhakar A, Krishnan V, Kunjukutty R, Vaidyanathan B. Clinical presentation, management, and postnatal outcomes of fetal tachyarrhythmias: A 10-year single-center experience. Ann Pediatr Cardiol. 2018 Jan-Apr;11(1):34-39. [PMC free article: PMC5803975] [PubMed: 29440828]
2.: Brubaker S, Long B, Koyfman A. Alternative Treatment Options for Atrioventricular-Nodal-Reentry Tachycardia: An Emergency Medicine Review. J Emerg Med. 2018 Feb;54(2):198-206. [PubMed: 29239759]
3.: Lundqvist CB, Potpara TS, Malmborg H. Supraventricular Arrhythmias in Patients with Adult Congenital Heart Disease. Arrhythm Electrophysiol Rev. 2017 Jun;6(2):42-49. [PMC free article: PMC5517371] [PubMed: 28835834]
4.: Massari F, Scicchitano P, Potenza A, Sassara M, Sanasi M, Liccese M, Ciccone MM, Caldarola P. Supraventricular tachycardia, pregnancy, and water: A new insight in lifesaving treatment of rhythm disorders. Ann Noninvasive Electrocardiol. 2018 May;23(3):e12490. [PMC free article: PMC6931545] [PubMed: 28833859]
5.: Corwin DJ, Scarfone RJ. Supraventricular Tachycardia Associated With Severe Anemia. Pediatr Emerg Care. 2018 Apr;34(4):e75-e78. [PubMed: 28376069]
6.: Khurshid S, Choi SH, Weng LC, Wang EY, Trinquart L, Benjamin EJ, Ellinor PT, Lubitz SA. Frequency of Cardiac Rhythm Abnormalities in a Half Million Adults. Circ Arrhythm Electrophysiol. 2018 Jul;11(7):e006273. [PMC free article: PMC6051725] [PubMed: 29954742]
7.: Amara W, Montagnier C, Cheggour S, Boursier M, Gully C, Barnay C, Georger F, Deplagne A, Fromentin S, Mlotek M, Lazarus A, Taïeb J., SETAM Investigators. Early Detection and Treatment of Atrial Arrhythmias Alleviates the Arrhythmic Burden in Paced Patients: The SETAM Study. Pacing Clin Electrophysiol. 2017 May;40(5):527-536. [PubMed: 28244117]
8.: Ho RT. A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism? Heart Rhythm. 2017 Oct;14(10):1570-1573. [PubMed: 28965610]
9.: Tabing A, Harrell TE, Romero S, Francisco G. Supraventricular tachycardia diagnosed by smartphone ECG. BMJ Case Rep. 2017 Sep 11;2017 [PMC free article: PMC5612203] [PubMed: 28899884]
10.: L’Italien K, Conlon S, Kertesz N, Bezold L, Kamp A. Usefulness of Echocardiography in Children with New-Onset Supraventricular Tachycardia. J Am Soc Echocardiogr. 2018 Oct;31(10):1146-1150. [PubMed: 30076010]
11.: Jain D, Nigam P, Indurkar M, Chiramkara R. Clinical Significance of the Forsaken aVR in Evaluation of Tachyarrhythmias: A Reminder. J Clin Diagn Res. 2017 Jun;11(6):OM01-OM04. [PMC free article: PMC5535428] [PubMed: 28764236]
12.: Chung R, Wazni O, Dresing T, Chung M, Saliba W, Lindsay B, Tchou P. Clinical presentation of ventricular-Hisian and ventricular-nodal accessory pathways. Heart Rhythm. 2019 Mar;16(3):369-377. [PubMed: 30103070]
13.: Voerman JJ, Hoffe ME, Surka S, Alves PM. In-Flight Management of a Supraventricular Tachycardia Using Telemedicine. Aerosp Med Hum Perform. 2018 Jul 01;89(7):657-660. [PubMed: 29921358]
14.: Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger J., REVERT trial collaborators. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015 Oct 31;386(10005):1747-53. [PubMed: 26314489]
15.: Mironov NY, Golitsyn SP. [Overwiew of New Clinical Guidelines for the Diagnosis and Treatment of Supraventricular Tachycardias (2015) of the American College of Cardiology/American Heart Association/Society for Heart Rhythm Disturbances (ACC/AHA/HRS)]. Kardiologiia. 2016 Jul;56(7):84-90. [PubMed: 28290912]
16.: Ordonez RV. Monitoring the patient with supraventricular dysrhythmias. Nurs Clin North Am. 1987 Mar;22(1):49-59. [PubMed: 3644291]
17.: Balli S, Kucuk M, Orhan Bulut M, Kemal Yucel I, Celebi A. Transcatheter Cryoablation Procedures without Fluoroscopy in Pediatric Patients with Atrioventricular Nodal Reentrant Tachycardia: A Single-Center Experience. Acta Cardiol Sin. 2018 Jul;34(4):337-343. [PMC free article: PMC6066944] [PubMed: 30065572]
18.: Alsaied T, Baskar S, Fares M, Alahdab F, Czosek RJ, Murad MH, Prokop LJ, Divanovic AA. First-Line Antiarrhythmic Transplacental Treatment for Fetal Tachyarrhythmia: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2017 Dec 15;6(12) [PMC free article: PMC5779032] [PubMed: 29246961]
19.: Upadhyay S, Marie Valente A, Triedman JK, Walsh EP. Catheter ablation for atrioventricular nodal reentrant tachycardia in patients with congenital heart disease. Heart Rhythm. 2016 Jun;13(6):1228-37. [PubMed: 26804568]

Supraventricular Tachycardia – StatPearls – NCBI Bookshelf

Continuing Education Activity

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

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

Pathophysiology

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

Evaluation

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

Treatment / Management

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).

Differential Diagnosis

Atrial flutter
Atrial tachycardia
Atrial fibrillation
Ventricular tachycardia

Complications

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

Pearls and Other Issues

Enhancing Healthcare Team Outcomes

Outcomes

Figure

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

Figure

References

1.: Karmegeraj B, Namdeo S, Sudhakar A, Krishnan V, Kunjukutty R, Vaidyanathan B. Clinical presentation, management, and postnatal outcomes of fetal tachyarrhythmias: A 10-year single-center experience. Ann Pediatr Cardiol. 2018 Jan-Apr;11(1):34-39. [PMC free article: PMC5803975] [PubMed: 29440828]
2.: Brubaker S, Long B, Koyfman A. Alternative Treatment Options for Atrioventricular-Nodal-Reentry Tachycardia: An Emergency Medicine Review. J Emerg Med. 2018 Feb;54(2):198-206. [PubMed: 29239759]
3.: Lundqvist CB, Potpara TS, Malmborg H. Supraventricular Arrhythmias in Patients with Adult Congenital Heart Disease. Arrhythm Electrophysiol Rev. 2017 Jun;6(2):42-49. [PMC free article: PMC5517371] [PubMed: 28835834]
4.: Massari F, Scicchitano P, Potenza A, Sassara M, Sanasi M, Liccese M, Ciccone MM, Caldarola P. Supraventricular tachycardia, pregnancy, and water: A new insight in lifesaving treatment of rhythm disorders. Ann Noninvasive Electrocardiol. 2018 May;23(3):e12490. [PMC free article: PMC6931545] [PubMed: 28833859]
5.: Corwin DJ, Scarfone RJ. Supraventricular Tachycardia Associated With Severe Anemia. Pediatr Emerg Care. 2018 Apr;34(4):e75-e78. [PubMed: 28376069]
6.: Khurshid S, Choi SH, Weng LC, Wang EY, Trinquart L, Benjamin EJ, Ellinor PT, Lubitz SA. Frequency of Cardiac Rhythm Abnormalities in a Half Million Adults. Circ Arrhythm Electrophysiol. 2018 Jul;11(7):e006273. [PMC free article: PMC6051725] [PubMed: 29954742]
7.: Amara W, Montagnier C, Cheggour S, Boursier M, Gully C, Barnay C, Georger F, Deplagne A, Fromentin S, Mlotek M, Lazarus A, Taïeb J., SETAM Investigators. Early Detection and Treatment of Atrial Arrhythmias Alleviates the Arrhythmic Burden in Paced Patients: The SETAM Study. Pacing Clin Electrophysiol. 2017 May;40(5):527-536. [PubMed: 28244117]
8.: Ho RT. A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism? Heart Rhythm. 2017 Oct;14(10):1570-1573. [PubMed: 28965610]
9.: Tabing A, Harrell TE, Romero S, Francisco G. Supraventricular tachycardia diagnosed by smartphone ECG. BMJ Case Rep. 2017 Sep 11;2017 [PMC free article: PMC5612203] [PubMed: 28899884]
10.: L’Italien K, Conlon S, Kertesz N, Bezold L, Kamp A. Usefulness of Echocardiography in Children with New-Onset Supraventricular Tachycardia. J Am Soc Echocardiogr. 2018 Oct;31(10):1146-1150. [PubMed: 30076010]
11.: Jain D, Nigam P, Indurkar M, Chiramkara R. Clinical Significance of the Forsaken aVR in Evaluation of Tachyarrhythmias: A Reminder. J Clin Diagn Res. 2017 Jun;11(6):OM01-OM04. [PMC free article: PMC5535428] [PubMed: 28764236]
12.: Chung R, Wazni O, Dresing T, Chung M, Saliba W, Lindsay B, Tchou P. Clinical presentation of ventricular-Hisian and ventricular-nodal accessory pathways. Heart Rhythm. 2019 Mar;16(3):369-377. [PubMed: 30103070]
13.: Voerman JJ, Hoffe ME, Surka S, Alves PM. In-Flight Management of a Supraventricular Tachycardia Using Telemedicine. Aerosp Med Hum Perform. 2018 Jul 01;89(7):657-660. [PubMed: 29921358]
14.: Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger J., REVERT trial collaborators. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015 Oct 31;386(10005):1747-53. [PubMed: 26314489]
15.: Mironov NY, Golitsyn SP. [Overwiew of New Clinical Guidelines for the Diagnosis and Treatment of Supraventricular Tachycardias (2015) of the American College of Cardiology/American Heart Association/Society for Heart Rhythm Disturbances (ACC/AHA/HRS)]. Kardiologiia. 2016 Jul;56(7):84-90. [PubMed: 28290912]
16.: Ordonez RV. Monitoring the patient with supraventricular dysrhythmias. Nurs Clin North Am. 1987 Mar;22(1):49-59. [PubMed: 3644291]
17.: Balli S, Kucuk M, Orhan Bulut M, Kemal Yucel I, Celebi A. Transcatheter Cryoablation Procedures without Fluoroscopy in Pediatric Patients with Atrioventricular Nodal Reentrant Tachycardia: A Single-Center Experience. Acta Cardiol Sin. 2018 Jul;34(4):337-343. [PMC free article: PMC6066944] [PubMed: 30065572]
18.: Alsaied T, Baskar S, Fares M, Alahdab F, Czosek RJ, Murad MH, Prokop LJ, Divanovic AA. First-Line Antiarrhythmic Transplacental Treatment for Fetal Tachyarrhythmia: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2017 Dec 15;6(12) [PMC free article: PMC5779032] [PubMed: 29246961]
19.: Upadhyay S, Marie Valente A, Triedman JK, Walsh EP. Catheter ablation for atrioventricular nodal reentrant tachycardia in patients with congenital heart disease. Heart Rhythm. 2016 Jun;13(6):1228-37. [PubMed: 26804568]

Supraventricular Tachycardia – StatPearls – NCBI Bookshelf

Continuing Education Activity

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

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

Pathophysiology

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

Evaluation

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

Treatment / Management

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).

Differential Diagnosis

Atrial flutter
Atrial tachycardia
Atrial fibrillation
Ventricular tachycardia

Complications

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

Pearls and Other Issues

Enhancing Healthcare Team Outcomes

Outcomes

Figure

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

Figure

References

1.: Karmegeraj B, Namdeo S, Sudhakar A, Krishnan V, Kunjukutty R, Vaidyanathan B. Clinical presentation, management, and postnatal outcomes of fetal tachyarrhythmias: A 10-year single-center experience. Ann Pediatr Cardiol. 2018 Jan-Apr;11(1):34-39. [PMC free article: PMC5803975] [PubMed: 29440828]
2.: Brubaker S, Long B, Koyfman A. Alternative Treatment Options for Atrioventricular-Nodal-Reentry Tachycardia: An Emergency Medicine Review. J Emerg Med. 2018 Feb;54(2):198-206. [PubMed: 29239759]
3.: Lundqvist CB, Potpara TS, Malmborg H. Supraventricular Arrhythmias in Patients with Adult Congenital Heart Disease. Arrhythm Electrophysiol Rev. 2017 Jun;6(2):42-49. [PMC free article: PMC5517371] [PubMed: 28835834]
4.: Massari F, Scicchitano P, Potenza A, Sassara M, Sanasi M, Liccese M, Ciccone MM, Caldarola P. Supraventricular tachycardia, pregnancy, and water: A new insight in lifesaving treatment of rhythm disorders. Ann Noninvasive Electrocardiol. 2018 May;23(3):e12490. [PMC free article: PMC6931545] [PubMed: 28833859]
5.: Corwin DJ, Scarfone RJ. Supraventricular Tachycardia Associated With Severe Anemia. Pediatr Emerg Care. 2018 Apr;34(4):e75-e78. [PubMed: 28376069]
6.: Khurshid S, Choi SH, Weng LC, Wang EY, Trinquart L, Benjamin EJ, Ellinor PT, Lubitz SA. Frequency of Cardiac Rhythm Abnormalities in a Half Million Adults. Circ Arrhythm Electrophysiol. 2018 Jul;11(7):e006273. [PMC free article: PMC6051725] [PubMed: 29954742]
7.: Amara W, Montagnier C, Cheggour S, Boursier M, Gully C, Barnay C, Georger F, Deplagne A, Fromentin S, Mlotek M, Lazarus A, Taïeb J., SETAM Investigators. Early Detection and Treatment of Atrial Arrhythmias Alleviates the Arrhythmic Burden in Paced Patients: The SETAM Study. Pacing Clin Electrophysiol. 2017 May;40(5):527-536. [PubMed: 28244117]
8.: Ho RT. A narrow complex tachycardia with atrioventricular dissociation: What is the mechanism? Heart Rhythm. 2017 Oct;14(10):1570-1573. [PubMed: 28965610]
9.: Tabing A, Harrell TE, Romero S, Francisco G. Supraventricular tachycardia diagnosed by smartphone ECG. BMJ Case Rep. 2017 Sep 11;2017 [PMC free article: PMC5612203] [PubMed: 28899884]
10.: L’Italien K, Conlon S, Kertesz N, Bezold L, Kamp A. Usefulness of Echocardiography in Children with New-Onset Supraventricular Tachycardia. J Am Soc Echocardiogr. 2018 Oct;31(10):1146-1150. [PubMed: 30076010]
11.: Jain D, Nigam P, Indurkar M, Chiramkara R. Clinical Significance of the Forsaken aVR in Evaluation of Tachyarrhythmias: A Reminder. J Clin Diagn Res. 2017 Jun;11(6):OM01-OM04. [PMC free article: PMC5535428] [PubMed: 28764236]
12.: Chung R, Wazni O, Dresing T, Chung M, Saliba W, Lindsay B, Tchou P. Clinical presentation of ventricular-Hisian and ventricular-nodal accessory pathways. Heart Rhythm. 2019 Mar;16(3):369-377. [PubMed: 30103070]
13.: Voerman JJ, Hoffe ME, Surka S, Alves PM. In-Flight Management of a Supraventricular Tachycardia Using Telemedicine. Aerosp Med Hum Perform. 2018 Jul 01;89(7):657-660. [PubMed: 29921358]
14.: Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger J., REVERT trial collaborators. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015 Oct 31;386(10005):1747-53. [PubMed: 26314489]
15.: Mironov NY, Golitsyn SP. [Overwiew of New Clinical Guidelines for the Diagnosis and Treatment of Supraventricular Tachycardias (2015) of the American College of Cardiology/American Heart Association/Society for Heart Rhythm Disturbances (ACC/AHA/HRS)]. Kardiologiia. 2016 Jul;56(7):84-90. [PubMed: 28290912]
16.: Ordonez RV. Monitoring the patient with supraventricular dysrhythmias. Nurs Clin North Am. 1987 Mar;22(1):49-59. [PubMed: 3644291]
17.: Balli S, Kucuk M, Orhan Bulut M, Kemal Yucel I, Celebi A. Transcatheter Cryoablation Procedures without Fluoroscopy in Pediatric Patients with Atrioventricular Nodal Reentrant Tachycardia: A Single-Center Experience. Acta Cardiol Sin. 2018 Jul;34(4):337-343. [PMC free article: PMC6066944] [PubMed: 30065572]
18.: Alsaied T, Baskar S, Fares M, Alahdab F, Czosek RJ, Murad MH, Prokop LJ, Divanovic AA. First-Line Antiarrhythmic Transplacental Treatment for Fetal Tachyarrhythmia: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2017 Dec 15;6(12) [PMC free article: PMC5779032] [PubMed: 29246961]
19.: Upadhyay S, Marie Valente A, Triedman JK, Walsh EP. Catheter ablation for atrioventricular nodal reentrant tachycardia in patients with congenital heart disease. Heart Rhythm. 2016 Jun;13(6):1228-37. [PubMed: 26804568]

Paroxysmal Supraventricular Tachycardia (PSVT) | Johns Hopkins Medicine

Paroxysmal supraventricular tachycardia (PSVT) is a type of abnormal heart rhythm, or arrhythmia. It occurs when a short circuit rhythm develops in the upper chamber of the heart. This results in a regular but rapid heartbeat that starts and stops abruptly.

What happens during PSVT?

A normal heartbeat begins with an electrical impulse from the sinus node, a small area in the heart’s right atrium (upper chamber). PSVT occurs because of a short circuit — an abnormal electrical pathway made of heart cells — that allows electricity to speed around in a circle and repeat the signal over and over. As a result, the chambers contract rapidly, which may impair heart function and cause symptoms such as lightheadedness or shortness of breath.

What causes PSVT?

The short circuit is caused by one of three conditions and will have a different location and behavior depending on the cause.

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)

Atrioventricular nodal re-entrant tachycardia (AVNRT) is the most common cause of PSVT. It occurs when a small extra pathway exists in or near the AV node — the “gate” that sends electricity from the upper chambers (atria) to the lower chambers (ventricles). An electrical impulse that enters this pathway will circle rapidly, causing a sudden (paroxysmal), fast heartbeat in both the atria and the ventricles. AVNRT is not a life-threatening arrhythmia, but it can cause symptoms such as lightheadedness or syncope (fainting).

Wolff-Parkinson-White Syndrome (WPW)

Wolff-Parkinson-White syndrome occurs when an extra muscle fiber connects the upper and lower chambers of the heart. In normal hearts, the only connection between the upper and lower chambers is the AV node — the electrical signal passes from the atria, through the AV node, and ends in the ventricles. The presence of this extra path can encourage a “short circuit” arrhythmia known as an atrioventricular reciprocating tachycardia (AVRT). The symptoms of AVRT vary widely from mild heart racing to syncope. Due to an increased risk of sudden cardiac death, people with Wolfe-Parkinson White syndrome are advised to have curative catheter ablation.

Wolff-Parkinson-White syndrome is congenital, developing in utero. Although present from birth, the tachycardias (rapid heartbeats) that result from the abnormal electrical connection often take years or decades before they become a problem.

Atrial Tachycardia

Atrial tachycardia is responsible for about 5 percent of PSVTs. It occurs when an electrical impulse fires rapidly from a site outside the sinus node and circles the atria, often due to a short circuit.

What are the symptoms of PSVT?

PSVT is often misdiagnosed as a panic attack. Symptoms include:

A regular but racing heartbeat of 120 to 230 beats per minute that starts and stops abruptly
Palpitations (a feeling of fluttering in the chest)
Weakness or fatigue
Dizziness or lightheadedness
Fainting (syncope)
Chest pain

How is PSVT diagnosed?

Doctors often suspect PSVT after a careful medical history and review of a 12-lead electrocardiogram (ECG or EKG). But because PSVT is paroxysmal (occasional and sudden), an office ECG may look normal. To “catch” an episode, your doctor may give you an ECG monitor to wear at home that will record your heart rhythm over time. These include:

Holter monitor: a portable ECG you wear continuously for one to seven days to record your heart rhythms over time
Event monitor: a portable ECG you wear for one or two months, which records only when triggered by an abnormal heart rhythm or when you manually activate it
Implantable monitor: a tiny event monitor inserted under your skin, worn for several years to record events that only seldom take place

However, the ultimate test of PSVT is an electrophysiological (EP) study. This test not only diagnoses the condition but also identifies the precise cause. A diagnostic EP study is always done before catheter ablation, usually as part of the same procedure. With the patient under light sedation, several narrow, flexible wires are threaded through a vein to your heart. Fine wires inside the catheter can help pinpoint any areas outside the sinus node that produce electrical signals, then remove them using catheter ablation.

How is PSVT treated?

Valsalva maneuver: In many patients, the tachycardia episode can be stopped by bearing down or rubbing the carotid artery.
Medications: Different types of medications are available, which vary in frequency, side effects, risks and efficacy. Because PSVT does not resolve on its own, medications would be taken for a lifetime.
Catheter ablation: This outpatient procedure is used to treat or cure many types of heart arrhythmia, including PSVT. Catheter ablation is a mature technique known to be safe and effective. Therefore, it is considered a first-line therapy for PSVT. It is often reasonable to go straight to catheter ablation rather than trying a medication first.

Learn more about arrhythmias or visit the Johns Hopkins Electrophysiology and Arrhythmia Service.

Supraventricular Tachycardia – an overview

Electrophysiological Differential Diagnosis of Focal Atrial Tachycardia

Atrial tachycardias, particularly those originating from the septal region, must be differentiated from concealed septal bypass tract–mediated tachycardia (i.e., orthodromic reciprocating tachycardia), atrioventricular node reentry tachycardia (AVNRT) and its variants, and other rare entities such as concealed nodoventricular or nodofascicular pathways. One of the most useful electrocardiographic or electrophysiological findings is AV block during tachycardia; when it occurs, a concealed bypass tract is eliminated as a diagnostic possibility.

Adenosine administration is a useful diagnostic tool in patients with supraventricular tachycardia.⁸⁶ In a report from Scheinman et al., 229 patients with supraventricular tachycardia during an electrophysiology study received intravenous boluses of 6 to 18 mg of adenosine. For patients with AT (n = 53), no consistent correlation was found between the response to adenosine and the location of the atrial focus. Termination or suppression of tachycardia with adenosine was observed in 56% of patients, but was not helpful for differentiating automatic tachycardias from triggered or reentrant tachycardias. Only patients with ATs demonstrated atrial cycle length oscillations (23%) before suppression with adenosine. AV block after adenosine was observed only in patients with AT, but it occurred uncommonly, being noted in only 27% of patients. Termination of AT renders the presence of a macroreentrant AT highly unlikely.

A variety of pacing maneuvers have been reported to be useful for the differentiation of AT from other forms of supraventricular tachycardia^87,88 (Tables 73-1, 73-2). Ventricular pacing can be useful for differentiating AT from AV nodal reentry tachycardia and AV reentry tachycardia. Ventricular burst pacing for at least 3 to 6 beats at a cycle length shorter than the tachycardia cycle length results in tachycardia termination, entrainment of the tachycardia, or dissociation of the ventricle from the tachycardia. If the ventricle is dissociated from the tachycardia, a bypass tract is excluded. If burst pacing reproducibly terminates tachycardia without conduction to the atrium, AT is excluded as the mechanism.

Burst pacing sometimes can be performed from the right ventricle for longer periods at a cycle length just shorter than the tachycardia cycle length. When atrial activation is accelerated to the pacing rate with 1 : 1 ventriculoatrial conduction, and if the atrial activation sequence during pacing is different from that during tachycardia, then either an AT or a bystander accessory pathway is present. When ventricular pacing is stopped and the electrogram sequence following the last paced ventricular beat demonstrates a V-A-A-V response (i.e., the last atrial complex accelerated to the pacing rate is followed by another atrial complex before the next ventricular complex), an AT is present. This finding is apparent because, following cessation of ventricular overdrive pacing during an AT, the last entrained atrial depolarization cannot conduct in an anterograde manner because the AV node is refractory after recent retrograde conduction; this results in two atrial depolarizations between ventricular depolarizations (V-A-A-V response). A “pseudo” V-A-A-V response may be seen in patients with slowly conducting septal accessory pathways or AV node reentry, particularly of the fast-slow or slow-slow types. A “V-A-H-A-V” sequence also may be seen with AV nodal reentry.

Delivering a ventricular extrastimulus during tachycardia might also provide diagnostic clues to the mechanism of an SVT. Any effect with a ventricular extrastimulus when the His bundle is refractory, including tachycardia termination without depolarizing the atrium, atrial preexcitation, or paradoxical delay of the subsequent atrial response excludes a diagnosis of AT.

Atrial pacing maneuvers also can be helpful to differentiate the various forms of supraventricular tachycardia. Overdrive pacing of the right atrium during tachycardia at a cycle length slightly shorter than the tachycardia cycle length can result in tachycardia termination (diagnostic maneuver not helpful) or tachycardia continuation upon cessation of pacing. If the V-A interval of the return cycle is within 10 ms of the V-A interval during the tachycardia, then the tachycardia is due to AV nodal reentry or a bypass tract. If the V-A interval is variable or different after pacing ceases, then AT is present. A second maneuver is atrial overdrive pacing during tachycardia at the longest cycle length, which results in AV block. The last paced atrial-His bundle (A-H) interval upon cessation of pacing is evaluated. If termination of the tachycardia is associated with a relatively short A-H interval compared with the A-H intervals that resulted in continuation of the tachycardia, then the tachycardia is considered to be AV node dependent and cannot be an AT. Another useful maneuver is to compare the A-H interval during tachycardia and atrial pacing from the high right atrium at or near the tachycardia cycle length. If the A-H interval during atrial pacing at the tachycardia cycle length is more than 40 ms longer than the A-H interval during tachycardia, atypical AV nodal reentry is much more likely. The A-H intervals during atrial pacing and tachycardia will be within 20 ms for ATs and concealed bypass tracts. Atrial pacing should be performed as soon as possible after tachycardia termination.

Tachycardia cycle length variability of 15 ms or more associated with a change in atrial cycle length that predicts a change in ventricular cycle length favors either AT or atypical AVNRT. A change in atrial cycle length that is preceded by the change in the preceding cycle length or H-H interval is suggestive of AVNRT or orthodromic reciprocating tachycardia.⁸⁹

The postpacing interval response to atrial overdrive pacing during tachycardia also may be useful to localize the site of origin of focal AT. Mohamed et al.⁹⁰ performed atrial overdrive pacing during AT at a rate slighter faster than the tachycardia rate. Measurement of the postpacing interval minus the tachycardia cycle length (PPI-TCL) from various sites in the right and left atria localized the tachycardia focus when the PPI-TCL was minimized (e.g., for the successful ablation site, 11 ± 8 ms). The investigators explained this observation by hypothesizing that the difference between the PPI and the TCL was proportional to the distance of the pacing site to the tachycardia focus and conduction time through the surrounding or perifocal tissue. In this study, overdrive suppression of the AT focus was not apparent. The PPI-TCL was never greater than 20 ms at a successful ablation site, suggesting minimal slowing by tissue near the atrial focus.

Supraventricular Tachycardia – Causes, Signs and Symptoms

Causes

There are different forms of supraventricular tachycardia (SVT), an abnormal fast heart rhythm. At times, thyroid disease, caffeine, medications with stimulants, or stress can cause an episode of SVT. However, often no trigger is identified.

Remember that your heart has a system of electrical impulses that helps control the rhythm and number of times your heart beats per minute. The electrical signals travel along “pathways.” Some types of SVT involve a faulty electrical pathway. Examples include:

Atrioventricular Nodal Reentrant Tachycardia (AVNRT): With AVNRT, the most common form of supraventricular tachycardia, there is a slow pathway in the middle of the heart. An extra beat timed just right sets off a circuit by going down the slow pathway and then going up a fast pathway. This loops around many times and creates a fast heart rate.

Wolff-Parkinson-White syndrome (WPW): With WPW, there is an extra pathway between the upper and bottom chambers of the heart. A circuit can be created with an extra beat going down the normal path and then up this extra pathway. It can go backward as well. Either way, this loops around many times creating a fast heart rate.

Atrial Tachycardia (AT): With atrial tachycardia, a cluster of cells in the upper chamber of the heart fires away, creating a rapid heartbeat.

Signs and symptoms

With SVT, your heart beats very fast for reasons other than stress or exercise. Often, you will notice a sudden increase in your heart rate ( > 100 beats per minute and even rates of > 200 beats per minute). Then, it suddenly returns to normal (about 60-100 beats per minute).

Depending on how fast the heart is beating, the symptoms can include:

Palpitations
Lightheadedness
Passing out
Sweating
Chest pain
Shortness of breath

Supraventricular Tachycardia | Circulation

The heart is a 4-chambered muscle that functions as a blood pump; the 2 upper chambers are called the atria and the 2 lower chambers are the ventricles. The rhythm of the heart is normally controlled by a natural pacemaker (the sinoatrial node) in the right upper chamber that beats about 60 times per minute at rest and can increase with exercise. Electrical impulses travel from the natural pacemaker through the atria, then pass through a filter called the atrioventricular node (AV) between the atria and ventricles before running down specialized fibers that activate the ventricles. (Figure 1)

Figure 1. Diagram of the heart and the electrical conduction system of the heart. Electrical impulses start in the sino-atrial node and travel via the atria to the AV node. From there, the electrical impulse travels through the His fibers and the Purkinje fibers to the left and right ventricles.

The atria are above the ventricles, hence the term supraventricular. The term tachycardia refers to a rapid heartbeat of over 100 beats per minute. Supraventricular tachycardia is frequently abbreviated as SVT (formerly paroxysmal atrial tachy- cardia or PAT). Supraventricular tachycardia then is a rapid rhythm of the heart that begins in the upper chambers. When patients experience change in the normal sequence of electrical impulses and an abnormal heart rhythm occurs, they are said to be having an arrhythmia.

Symptoms During Supraventricular Tachycardia

Palpitations
Lightheadedness
Dizziness
Loss of consciousness
Chest pain
Shortness of breath

Typically, patients have symptoms from SVT, but occasionally they may have no symptoms. A common symptom during SVT is palpitations or a sensation that the heart is beating rapidly, fluttering, or racing. This may last for a few seconds or several hours. Occasionally, patients may have a sensation of shortness of breath or “air-hunger,” or chest pressure or pain. Sometimes patients will feel lightheaded or dizzy, and rarely patients will feel like they are about to pass out. Loss of consciousness (also known as syncope) during SVT is a rare occurrence. Although such symptoms may raise concern, in general, SVT is not a serious or life-threatening condition. Nonetheless, if any of these symptoms develops, immediate medical attention should be sought.

How Is Supraventricular Tachycardia Diagnosed?

The electrocardiogram (ECG or EKG) provides a picture of the heart rhythm and is recorded by placing adhesive or gel pads on the chest and limbs. If the patient is experiencing SVT during the ECG, a clear diagnosis can be made. Various other types of electrocardiographic monitors may be used to record the patient’s heart rhythm to help make a diagnosis of SVT. A 24-hour ambulatory Holter monitor may be used to record the heart rhythm continuously for 24 hours. This type of monitor is particularly helpful in documenting asymptomatic or very frequent rhythm abnormalities. For those patients whose arrhythmias occur relatively infrequently, event or loop monitors may be worn. An event monitor is attached to the patient’s wrist or chest whenever symptoms suggesting SVT occur. Activating a button on the monitor will start a recording of the heart’s rhythm. The patient is given instructions about how to download this information to a computer that stores results for later analysis via a special device placed over a telephone mouthpiece. For patients who experience very brief arrhythmias or those accompanied by severe lightheadedness, an event monitor is impractical. In such cases, patients may wear a loop monitor continuously for days to weeks. The loop monitor continuously records the heart’s rhythm so that the patient need only press a button to save a record of the rhythm during the preceding and subsequent 1 to 2 minutes. This permits recording even very transient arrhythmias. The loop monitor record is downloaded using a telephone in the same way that event monitor data are transmitted.

How Is Supraventricular Tachycardia Classified?

An SVT is classified medically on the basis of the path that the electrical signal takes from the atria. One type of SVT (AV nodal reentrant tachycardia or AVNRT) occurs because the electrical impulse travels in a circle using extra fibers in and around the AV node (Figure 2). Another type of SVT occurs because of electrical conduction via extra fibers between the atria and ventricles; this means of conduction is called a bypass tract or accessory pathway. The electrical impulse travels down the AV node to the ventricle and back to the atrium via these extra fibers, producing the SVT called AV reentrant tachycardia, or AVRT (Figure 3). Some patients are told that they have Wolff-Parkinson-White Syndrome (WPW), in which there is evidence of conduction via an accessory pathway from the atrium to the ventricle that may be detected on the ECG even if they are not experiencing SVT. Atrial tachycardias occur when localized regions in the atria develop the ability to fire rapidly on their own.

Figure 2. Diagram of AV nodal reentrant tachycardia (AVNRT). The electrical impulse travels in a circle using extra fibers in and around the AV node.

Figure 3. A diagram of AV reentrant tachycardia (AVRT). The electrical impulse travels down the AV node to the ventricles and back to the atrium via extra fibers that connect the atria and ventricles.

How Is Supraventricular Tachycardia Treated?

Medications may be used to treat many patients with SVT. The most commonly used classes of medications are:

β-blockers: These are commonly used to treat high blood pressure and other heart problems such as angina. In SVT, they are used specifically to decrease conduction through the AV node (Figure 1) to stop conduction during the tachycardia.
Calcium channel blockers: These are also used to treat high blood pressure and heart problems. Like β-blockers, they may be used to decrease conduction through the AV node. Examples of calcium channel blockers include verapamil or diltiazem.
Antiarrhythmic agents: These agents are used to treat various arrhythmias and directly affect the atrial or ventricular heart tissue. They are most useful in SVTs that use an accessory pathway or bypass tract or in atrial tachycardias.

You will want to discuss with your physician the medical therapy that is right for you.

A special procedure called radiofrequency ablation (RFA) has been developed as an alternative to medication to treat many patients with SVT. During this procedure, special plastic tubes called catheters are inserted into a vein into the upper leg/groin area and are advanced to the heart using a fluoroscope. The catheters are used to record electrical signals from inside the heart. They can locate precisely the site from which the SVT originates. Radio waves (called radiofrequency energy) are delivered at the tip of this catheter to the precise location of the SVT, creating a small coagulation of the tissue approximately 2 mm in diameter. The procedure has a 90% to 95% chance of successfully treating the SVT, so that it does not recur or require medication. There is approximately a 5% chance that the SVT will recur, usually within the first 1 to 2 months.

RFA can carry the risks described below:

Less than 1% risk of serious or life-threatening complications
Less than 1% risk of damage to the normal conduction system
Bleeding, bruising, or infection at catheter insertion site
Damage to the heart, lungs, blood vessels, or nerves
Blood clots to the lungs
Need for electrical shock to the chest
Rashes
Allergic reactions
Adverse effects of sedatives or anesthetic agents, such as respiratory depression requiring insertion of a breathing tube

Your cardiologist will discuss the complications and benefits of RFA with you and let you know if it is an appropriate treatment for your medical condition.

What Can I Do When I Develop Supraventricular Tachycardia?

You may want to discuss with your physician the steps that you may take when you develop SVT. For instance, your physician may instruct you to perform the Valsalva maneuver to try to stop the SVT yourself if you do not have lightheadedness, shortness of breath, chest pain, or other severe symptoms. To do this maneuver, first lie down, take a deep breath and hold it, and then bear down as if you are having a bowel movement.

If you become quite lightheaded, you should lie down and call for assistance and for immediate transport to a local hospital. If transportation is not immediately available, or if you have chest pain or feel like you might lose consciousness, call 911 right away. You may be brought to the emergency department of a local hospital. There, an ECG will be performed and an intravenous line will be started. You may be given a small amount of a medication called adenosine that is quite effective in stopping the SVT. Adenosine may cause flushing, a hot sensation, and a sudden feeling of breathlessness for 30 seconds or less. It should be used with caution in patients with asthma. Other medications such as verapamil, β-blockers, or diltiazem may also be given intravenously.

Footnotes

Correspondence to Paul J. Wang, MD, Tufts New England Medical Center, 750 Washington St, Boston, MA 02111. E-mail [email protected]

Additional Information

1 The North American Society of Pacing and Electrophysiology. Rapid heartbeat (tachycardia and fibrillation). Available at: http://www. naspe-patients.org/patients/signs_symptoms/too_fast.html. Accessed November 5, 2002.Google Scholar
2 National Heart, Lung, and Blood Institute. Facts about arrhythmias/rhythm disorders. Available at: http://www.nhlbi.nih.gov/health/public/heart/other/arrhyth.htm. Accessed November 5, 2002.Google Scholar
3 American Heart Association. Arrhythmia: patients and family. Available at: http://216.185.112.5/presenter.jhtml?identifier=8. Accessed November 5, 2002.Google Scholar
4 American Heart Association. Dr. Goodheart: Wolf-Parkinson-White syndrome. Available at: http://216.185.112.5/presenter.jhtml?identifier=1000. Accessed November 5, 2002.Google Scholar
5 American Heart Association. Arrhythmias. Available at: http://216.185.112.5/presenter. jhtml?identifier=11077. Accessed November 5, 2002.Google Scholar

Paroxysmal supraventricular tachycardia – treatment at the Federal Research Center for Medical and Biological Sciences of the Federal Medical and Biological Agency of Russia

Paroxysmal supraventricular tachycardia, abbreviated PNT, is a type of arrhythmia. Accompanied by a heart rate (HR) from 140 to 220 or more beats per minute. Occurs spontaneously and ends unexpectedly. The duration of PNT is at least three cardiac cycles, while maintaining a regular heart rate. The attack itself can last from a few seconds to several days.

PNT occurs due to a violation of the nervous regulation of cardiac activity or damage to other organs.

In the first case, excessive nerve stimulation leads to an increase in heart rate.

PNT can also occur in healthy people under the influence of certain factors:

prolonged physical activity;
stress;
the use of energy and stimulating drinks;
bad habits.

In the case of organic damage, paroxysmal supraventricular tachycardia can be caused by:

In addition to heart disease, other organs can affect paroxysmal supraventricular tachycardia.It is worth checking the functioning of the kidneys, lungs and gastrointestinal tract, especially if there are chronic or acute diseases.

Symptoms of paroxysmal supraventricular tachycardia

Paroxysmal tachycardia always has a sudden, distinct onset. The patient feels a jolt or squeeze, and sometimes a prick, in the area of the heart.

The attack may be accompanied by symptoms:

dizziness;
noise in the head;
light-headedness or fainting;
sweating;
nausea;
trembling in the body.

To correctly diagnose tachycardia, it is important to conduct a thorough interview and examination of the patient. Highly qualified doctors of the FNKTs FMBA Cardiology Center will be able to quickly identify the ailment.

Diagnostics

Tachycardia is sinus and paroxysmal, they differ from the place of origin of the electrical impulse, which causes the heart to contract. To make a diagnosis, the doctor of the FNKTs FMBA conducts a physical examination, collects an anamnesis and prescribes tests.

Physical examination includes:

external examination of the patient;
measuring heart rate;
blood pressure measurement.

Instrumental research:

ECG;
ECG with additional stress on the body;
daily ECG monitoring;
ECHO;
stress echocardiography;
MRI;
CT cardiography.

Prevention

Prevention consists of early diagnosis. Often, success directly depends on the patient and his attitude towards his health. The main recommendations that should be followed during prevention:

moderate regular physical activity;
proper nutrition;
rejection of bad habits;
avoiding stressful situations that cause anxiety;
compliance with the instructions of the attending physician.

The main thing is to diagnose tachycardia in a timely manner in order to switch to prevention in time. You can get acquainted with the programs of our center by the link.

How to treat paroxysmal supraventricular tachycardia

There are several treatment options at the FNKTs FMBA center. Depending on the degree of the ailment, the attending physician may place you in a therapy department. You will be under the constant supervision of professionals and receive timely medical assistance.This is usually drug therapy. If the symptoms of standard therapy are insufficient, then you may be offered catheter ablation of the arrhythmia. At the same time, by puncture access under local anesthesia, under X-ray control, using a catheter, an accurate diagnosis of the arrhythmia focus is performed and, by pointwise action on it with a radiofrequency pulse or cold, the cause of paroxysmal tachycardia is eliminated.

90,000 Diagnostics, treatment of paroxysmal tachycardia at the Clinical Hospital on Yauza, Moscow

02.11.2021

The article was checked by a cardiologist of the highest category Kurbatova I.V. is for general informational purposes only and does not replace specialist advice.
For recommendations on diagnosis and treatment, a doctor’s consultation is required.

In the Yauza Clinical Hospital, for paroxysmal tachycardia, a range of diagnostics is carried out – ECG, 24-hour ECG monitoring, echocardiography, according to indications – veloergometry, stress ECHO-KG, EFI – electrophysiological examination of the heart, CT coronary angiography, MRI of the heart, etc.Experienced cardiologists will select an effective drug therapy regimen. If necessary, surgical treatment is possible – radiofrequency ablation, implantation of a cardioverter-defibrillator, pacemaker, which are carried out by the leading cardiac surgeon prof. A.V. Ardashev.

Paroxysmal tachycardia is a paroxysmal increase in heart rate from 140 to 220 beats per minute or more. It occurs when the normal sinus (that is, set by the sinus node) rhythm is suppressed by a pathological source of impulses.If the source is located in the atria or in the transition from the atrium to the ventricles, they speak of supraventricular or supraventricular tachycardia. In the event that the source is in the ventricles of the heart, we are talking about ventricular tachycardia.

Make an appointment with a cardiologist

Reasons

Activation of the sympathetic nervous system, more often provokes supraventricular tachycardia, more often in young people.

Paroxysmal ventricular tachycardia usually occurs against the background of organic changes in the heart (coronary artery disease, heart attacks, inflammatory heart disease, cardiomyopathy).

Symptoms of paroxysmal tachycardia

Heartbeat attacks occur and end +, as a rule, suddenly.
Duration – from a few seconds to a day.
Attacks of paroxysmal tachycardia may be accompanied by signs of circulatory and cardiac insufficiency. These are dizziness, dizziness, shortness of breath, chest pain, drop in blood pressure.

Complications

With a prolonged attack, a drop in blood pressure, the development of acute heart failure, and pulmonary edema are possible.
Formation of blood clots in the heart that can cause heart attacks of vital organs – kidneys, lungs, brain (stroke).
Ventricular tachycardia can lead to cardiac arrest.

Diagnostics

Electrocadiography, including 24-hour Holter monitoring, exercise ECG – to identify the fact and type of arrhythmia.
Echocardiography, less often – MRI and CT examinations of the heart – to search for intracardiac causes of rhythm disturbances.
Additional studies according to an individually developed examination plan to identify non-cardiac causes of arrhythmias (laboratory tests, ultrasound, etc.).
According to indications – intracardiac electro-physiological examination (EPI) followed by surgical treatment of this type of arrhythmia.

Treatment

Emergency care for paroxysmal tachycardia. There are a number of ways to slow down the rhythm, called vagal tests, which are taught to the patient by a cardiologist.An urgent call to the emergency medical team is urgent.
Conservative therapy . Performed by experienced cardiologists. Individual selection of drugs for relief of paroxysmal tachycardia and prevention of seizures, as well as for reducing the risk of thrombus formation, improving myocardial condition, etc.
Surgical treatment . Depending on the patient’s condition and the nature of the seizures, various interventions are used: radiofrequency ablation of arrhythmogenic zones or implantation of a cardioverter-defibrillator.

In the Yauza Clinical Hospital, the decision on surgical intervention, its choice and the operation itself are made by the cardiac surgeon-arrhythmologist Professor A.V. Ardashev.

The cardiology department of our hospital carries out dynamic observation of patients with paroxysmal tachycardia and timely correction of their treatment, reducing the risk of dangerous conditions and complications.

Cost of services

Make an appointment

You can look at prices for services in the price list or check the phone number indicated on the website.

Reviews

Andrey

The state of health during attacks of paroxysmal tachycardia leaves much to be desired. and the complications of the disease cause panic and overwhelming fear. It is important to diagnose pathology in a timely manner in order to have time to choose an effective treatment. Thanks to the doctors of the clinic on Yauza for a quick and informative examination. Thanks to you, I have avoided dangerous complications and managed to stay healthy.

Alexander

I was sincerely delighted with the technical capabilities of the hospital.I never thought that in one hospital there can be so many different devices for detecting a disease. The professionalism of the doctors also gave the impression of no panic, no unnecessary movements. They quickly stopped the attack, prescribed examinations, identified the cause and even selected a treatment. I only feel great because of you.

Natalia

My attacks of paroxysmal tachycardia were usually accompanied by panic. And even after the seizure was over, it was difficult for me to explain to the doctor what happened to me.I am insanely grateful to the doctors of the clinic for being able to recognize the symptoms of the disease in my confused story and conduct a quality examination and still find the problem. Now after the treatment I feel great. I don’t want to think about how the situation would have ended if it were not for the cool diagnostic methods of your clinic.

Literature:

Fazio G., Mongiovi ‘M., Sutera L. Segmental dyskinesia in Wolff-Parkinson-White syndrome: a possible cause of dilatative cardiomyopathy // Int J Cardiol. 2008.
Khamnagadaev I.A., Shkolnikova M.A., Kokov L.S. Diastolic function of the right ventricle in patients with manifest syndrome and electrocardiographic phenomenon of Wolff-Parkinson-White // Herald of arrhythmology. 2012.

Terms and definitions / Consultant Plus

Terms and definitions

Supraventricular cardiac arrhythmias (NZHNRS) – a group of cardiac arrhythmias that differ in etiology, pathogenetic mechanisms, clinical and electrocardiographic manifestations and prognosis, the main unifying feature of which is the location of the arrhythmia source above the branches of the His bundle, namely in the AV junction, atria, orifices pulmonary / vena cava or sinus node cells.

Supraventricular extrasystole (ELE) is called premature (relative to normal, sinus rhythm) single or paired electrical activation of the heart caused by impulses originating in the atria, in the pulmonary / vena cava (where they enter the atrium) or in the AV- connection.

Accelerated supraventricular rhythm (UPVR) – three or more consecutive cardiac contractions occurring at a higher frequency than the normal sinus rhythm, but at the same time not exceeding 100 beats per minute, when the source of arrhythmia is located outside the sinus node, but above the branching of the His bundle, namely: in the atria, in the orifices of the pulmonary / vena cava or in the AV junction.

Supraventricular tachycardia (NSVT) – three or more consecutive cardiac contractions with a frequency of more than 100 per minute, provided that sinus node cells, atrial myocardium, muscle couplings of the pulmonary / vena cava and / or AV junction cells participate in the self-sustaining mechanism of arrhythmia.

Sinus tachycardia is defined as sinus rhythm greater than 100 per minute. Sinus tachycardia is a form of the body’s physiological response to physical and emotional stress, it is not a pathology.

Chronic inadequate sinus tachycardia is called persistent sinus tachycardia at rest (heart rate over 90-100 per minute) and / or an inadequately large increase in heart rate with minimal physical and emotional stress (for example, reaching submaximal heart rate values by age already at the first, minimum stage of the stress test ) in the absence of apparent reasons for this phenomenon.

Sinoatrial reciprocal tachycardia (SART) is a paroxysmal (paroxysmal) supraventricular tachycardia, the pathogenetic mechanism of which is a re-entry of an impulse (re-entry), which is realized in the sinus node and adjacent right atrial myocardium.

Atrial tachycardia (AT) – supraventricular tachycardia, an arrhythmogenic source (less often – several sources) of which is localized in the atrial myocardium and / or in the hollow / pulmonary veins flowing into them.

AV-nodal reciprocal tachycardia (AVURT) – paroxysmal supraventricular tachycardia, the pathogenetic mechanism of which is the circulation of impulses (re-entry) in the AV node and adjacent septal region of the atrial myocardium.

Preexcitation syndromes include a group of supraventricular tachycardias resulting from the presence of an abnormal, additional conduction pathway (Kent’s bundle or Mahaim fibers) with the possibility of anterograde and / or retrograde propagation of electrical impulses bypassing and, as a rule, ahead of the normal cardiac conduction system, which creates the phenomenon of premature excitation (pre-excitation) of the ventricles and / or atria.

Paroxysmal orthodromic reciprocal tachycardia (PORT) – paroxysmal supraventricular tachycardia, the pathogenetic mechanism of which is the circulation of impulses between the atria and ventricles, anterograde along the AV node and retrograde along the additional pathway (Kent’s bundle).

Paroxysmal antidromic reciprocal tachycardia (PART) – paroxysmal supraventricular tachycardia, the pathogenetic mechanism of which is the circulation of impulses between the atria and ventricles, anterograde along an additional pathway (Kent’s bundle or Mahaim fibers) and retrograde along the AV node.

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Subjective tolerance of paroxysmal supraventricular tachycardias (PNT) largely depends on the severity of tachycardia: at a heart rate (HR) of more than 130-140 beats / min, paroxysm rarely remains asymptomatic. However, sometimes patients do not feel the paroxysm of tachycardia, especially if the heart rate during the attack is low, the attack is short-lived, and the myocardium is intact.Some people experience a moderate heartbeat, but feel weak, dizzy, and nauseous during an attack. Generalized manifestations of autonomic dysfunction (tremors, chills, sweating, polyuria, etc.) with PNT are less pronounced than with attacks of sinus tachycardia.

The clinical picture to some extent depends on the specific type of arrhythmia, however, common to all PNT are complaints of a completely sudden onset of an attack of a sharp heartbeat.The rate of heart contractions, as it were, instantly switches from normal to very fast, which is sometimes preceded by a more or less long period of sensation of interruptions in the work of the heart (extrasystole). The end of a PNT attack is just as sudden as its onset, regardless of whether the attack stopped on its own or under the influence of drugs.

With very prolonged attacks, cardiovascular failure develops in most cases.

Auscultation during an attack reveals frequent rhythmic heart sounds; A heart rate of 150 beats / min and above excludes the diagnosis of sinus tachycardia, a heart rate of more than 200 makes ventricular tachycardia unlikely.It should be remembered about the possibility of atrial flutter with a conduction ratio of 2: 1, in which vagal tests can lead to a short-term deterioration in conduction (up to 3: 1, 4: 1) with a corresponding abrupt decrease in heart rate. If the duration of systole and diastole become approximately equal, the second tone in terms of volume and timbre becomes indistinguishable from the first (the so-called pendulum rhythm, or embryocardia). For most paroxysmal supraventricular tachycardias (PNT), rhythm rigidity is characteristic (its frequency is not influenced by intense breathing, physical activity, etc.).etc.).

However, auscultation does not allow to find out the source of tachycardia, and sometimes to distinguish sinus tachycardia from paroxysmal.

The pulse is frequent (often it is impossible to count it), soft, weak filling.

Occasionally, for example, with a combination of paroxysmal supraventricular tachycardia (PNT) and atrioventricular block II degree with periods of Samoilov-Wenckebach or with chaotic (multifocal) atrial tachycardia, the regularity of the rhythm is disturbed; in this case, the differential diagnosis with atrial fibrillation is possible only by ECG.

Blood pressure usually goes down. Sometimes the attack is accompanied by acute left ventricular failure (cardiac asthma, pulmonary edema).

Atrioventricular nodal reciprocal tachycardia (AVURT)

Atrioventricular nodal reciprocal tachycardia (AVRT)

Atrioventricular nodal reciprocal tachycardia (AVRT) is a supraventricular tachyarrhythmia with a re-entry mechanism using approaches to the atrioventricular (AV) node and a compact AV node.Pulse with tachycardia, as a rule, is in the range of 140-250 beats / min.

Epidemiology

AVURT is the most common form of supraventricular tachyarrhythmia (SVT) and is usually not associated with structural heart disease.

Prevalence

Approximately 70% of AVNRT patients are women. In women, AVURT first begins to manifest itself at a younger age (29 ± 16 years) than in men (39 ± 16 years). Concomitant organic heart disease occurs in only about 15% of cases.

The reasons why AVURT develops more often in women than in men are unclear. Cabrera J.A. et al (1998) observed in patients with AVURT the anatomical features of the structure of the heart (a wide coronary sinus, which takes a funnel-shaped form in venographic studies).

Classification and mechanisms

Schematic representation of the mechanism of AVURT formation.

AV-nodal conduction is functionally divided into fast and slow conduction paths with different electrophysiological properties.Different electrophysiological properties of the two groups of fibers in this area are the basis for the formation of re-entry of excitation (reentry) and the existence of tachycardia. With an extraordinary contraction of the atria (for example, with an atrial extrasystole), there is a blockade of conduction in the fast part and an impulse is conducted through the slow channel through the bundle of His to the ventricles, and through the fast channel conduction goes back to the atria, and then back to the “slow” one. Thus, a reentry loop is formed, which underlies AVURT.

There are three main forms of AVURT. A typical AVURT uses a slow anterograde pathway and a fast retrograde pathway (slow-fast, or slow-fast type). Rare forms are fast-slow (fast-slow type) and slow-slow (slow-slow type) AVRT.

+ More about AVNRT mechanisms for specialists Initially, it was believed that the re-entry circle is limited to the compact part of the atrioventricular node, but later there was evidence that the perinodal atrial tissue is a constituent part of the re-entry loop.However, it has been shown that AVNRT can exist without the participation of atrial tissue. For AVNRT to occur, two functionally and anatomically different channels are required. In most cases, the fast pathway is located near the tip of the Koch triangle. The slow path is located posteriorly and below the compact part of the pancreas and runs along the septal edge of the fibrous ring of the tricuspid valve at or just above the coronary sinus.

Diagram of the reentry circle with typical AV nodal reciprocal tachycardia

During a typical AVRT, the slow pathway acts as the antegrade portion of the loop, while the fast channel is the retrograde knee (i.e.i.e. slow-fast re-entry of the atrioventricular node). An impulse along the slow channel is conducted through the bundle of His to the ventricles, and along the fast channel, conduction goes back to the atria, as a result of which a P wave appears with a duration of 40 ms, which is superimposed on the QRS complex or occurs immediately after it (less than 70 ms), which often leads to the appearance of pseudo-r ‘in lead V ₁.

In rare cases (5-10%), the tachycardia loop has the opposite direction, i.e. conduction is carried out antegrade along the fast channel and retrograde along the slow channel (fast-slow re-entry of the atrioventricular node, or atypical AVNRT), leading to the appearance of a long R-P interval.The P wave, negative in leads III and aVF, is recorded in front of the QRS. There are rare cases when both parts of the tachycardia circle consist of slow-conducting tissue (slow-slow re-entry PZhU), the P´ wave is recorded after QRS (ie, the RP interval is greater than or equal to 70 ms).

Clinic AVURT

The disease proceeds in the form of attacks of rapid rhythmic heartbeat, which begins and stops suddenly. The duration of the AVURT paroxysm is from several seconds to several hours, and the frequency of their occurrence is from daily attacks of arrhythmias up to 1-2 times a year.Pulse with tachycardia, as a rule, is in the range of 140-250 beats / min. An AVURT attack is accompanied by palpitations, dizziness, throbbing in the neck.

Diagnostics

Electrocardiogram of patient N. during a typical AVNRT attack. Heart rate 170 bpm.

Electrocardiography (ECG) in 12 leads allows you to diagnose AVNRT. With normal sinus rhythm, the ECG usually does not show any changes. During an attack of a typical AVNRT, the ECG records tachycardia with a ventricular rate of 140 to 250 per minute.A 40 ms retrograde P wave overlaps or immediately follows the QRS complex (less than 70 ms), often resulting in a pseudo-r ‘in lead V ₁.

Electrophysiological research in modern cardiology is an absolute indication in patients with AVURT.

Treatment of an attack of tachyarrhythmia with AVNRT

An attack can be effectively stopped by carrying out reflex techniques (Valsalva test, massage of the carotid sinuses).From pharmacological agents, the drugs of choice are verapamil, adenosine, obzidan, novocainamide. Medicines can be administered orally or parenterally.

Treatment AVURT

Areas of influence on the slow (α) pathways of AV connections and the efficiency of arrhythmia elimination in various perinodal areas.

Today radiofrequency catheter ablation (RFA) AVURT is the most effective treatment for this arrhythmia, which allows the patient to completely stop taking antiarrhythmic drugs.The efficiency of RFA AVURT is 98-99%. Complications in the form of high-grade AV block with modification of the slow part by RFA occur in 1%. It is based on the destruction of the fibers of the “slow” part in the lower part of the Koch triangle. RFA AVURT is an absolute indication in patients with this arrhythmia. A contraindication to this operation is the patient’s preference for continuous antiarrhythmic therapy.

A number of antiarrhythmic drugs can be used to treat patients with frequent and persistent attacks of AVNRT who prefer continuous oral therapy and do not need catheter ablation.Standard therapy includes calcium channel blockers, beta-blockers, and digoxin. When treating patients without structural myocardial pathology who are resistant to drugs that slow down AV conduction, class Ic antiarrhythmic drugs – flecainide and propafenone are preferred. In most cases, Class III drugs such as sotalol or amiodarone are not used. Class Ia drugs – quinidine, procainamide and disopyramide are used to a limited extent, since they require a long-term administration regimen, have moderate efficacy and have a proarrhythmogenic effect.

Source:
Revishvili A.Sh. In the book: Bockeria L.A., Golukhova E.Z. (ed.) Clinical cardiology: diagnosis and treatment. M .: Publishing house NTsSSKh im. A.N. Bakuleva; 2011

Arrhythmology: Paroxysmal heart rhythm disturbances (tachycardia, tachyarrhythmias)

Paroxysmal (sudden onset) cardiac arrhythmias (ARRs) are the most common forms of arrhythmias. These LDCs can be independent or complicate the course of diseases of the cardiovascular system and other organs and systems.

Paroxysmal tachyarrhythmias are characterized by a sudden onset (and possibly ending) with the development of an attack of increased heart rate of more than 100 beats / min, the possible development of acute circulatory failure and require urgent treatment.

Tachyarrhythmias can occur anywhere in the heart.

Depending on the location of the focus, tachyarrhythmias are most often:

atrial (supraventricular),
ventricular,
sinus,
nodal,
atrioventricular.

The mechanism of occurrence of tachyarrhythmias can be different. Allocate the re-entry (reentry) mechanism – re-entry of the excitation wave, ectopic, trigger, etc. Separately, tachyarrhythmias with a wide or narrow QRS complex are distinguished, which determines further treatment tactics.

The most common in the population:

Supraventricular tachyarrhythmias (sinus, atrial, atrioventricular re-entry, atrial flutter, atrial fibrillation, etc.)) 90 105
Premature Ventricular Excitation Syndrome (WPW-Wolff-Parkinson-White Syndrome),
ventricular tachyarrhythmias.

The main symptoms of tachyarrhythmias (see cardiac arrhythmias and conduction disturbances)

Diagnosis of tachyarrhythmias

Usually, the diagnosis of tachyarrhythmias is carried out by a polyclinic doctor, cardiologist, ambulance doctor. It is important to take anamnesis, physical examination, and various instrumental and diagnostic methods.It is especially necessary to register an attack of tachyarrhythmia on an ECG (for presentation to an arrhythmologist). The Clinic has all the possible ways to diagnose and treat tachyarrhythmias.

The main ones include:

1. 12-lead ECG.
2. Daily, three-day and seven-day ECG monitoring.
3.Endocardial electrophysiological examination of the heart (endo-EPI) – carried out in a hospital. Endocardial EFI of the heart is performed in the X-ray operating room. This method makes it possible to assess the functional state of the cardiac conduction system and to find out the mechanism of arrhythmia occurrence, to determine the indications for radiofrequency catheter ablation (RFA) of additional conduction pathways and arrhythmogenic zones.

Treatment of tachyarrhythmias

For any rhythm disturbance, the influence of conditions such as the presence of thyrotoxicosis, alcohol abuse, smoking, imbalance in water and electrolyte balance, should be taken into account and excluded.and the presence of heart disease that can cause and maintain tachyarrhythmias.

There are several treatments for tachyarrhythmias:

1. Antiarrhythmic therapy (with constant medication).
2. Electrophysiological methods:

cardioversion / defibrillation;
electrocardiostimulation;
catheter ablation of the arrhythmia focus.

Catheter ablation (destruction) of the arrhythmia focus is a fairly effective and radical method of treatment. The operation, on average, lasts about 1 hour, and in a day the patient can be discharged from the hospital.

The choice of a method for treating a patient is carried out by a specialist taking into account the clinical picture of the disease, the data of instrumental and diagnostic studies and the recommendations of the All-Russian Scientific Society of Arrhythmologists, the All-Russian Scientific Society of Cardiology.Self-administration of drugs, self-medication by various methods is highly undesirable and unsafe given the unknown nature, mechanism and causes of tachycardia.

In the office of X-ray endovascular diagnostics and treatment of the Clinic of high medical technologies. NI Pirogov diagnostics of this type of LDC and catheter ablation for all types of tachycardia is carried out.

You can sign up for a consultation with a doctor – arrhythmologist by phone.8 812 676-25-25 or by filling out the form below

Sinus tachycardia of the heart – treatment, causes, symptoms

Author: doctor, scientific director of JSC “Vidal Rus”, Zhuchkova T.V., [email protected]

Table of contents:

Sinus tachycardia is a type of supraventricular tachyarrhythmia characterized by an accelerated sinus rhythm with a heart rate of more than 100 per minute in an adult.

Causes of sinus tachycardia

The causes of sinus tachycardia can be cardiac and non-cardiac factors.

Cardiac causes of tachycardia:

Heart failure
Cardiomyopathy and cardiosclerosis
Myocardial infarction
Myocarditis, endocarditis and pericarditis
Angina heart disease

Extracardiac causes of sinus tachycardia:

Physical activity
Emotional stress
Neuroses
Endocrine Disorders
Acute pain attacks
Fever
The use of certain drugs, such as vagolytics, corticosteroids, diuretics, and others.
Abuse of tea, coffee, alcohol and cigarettes

Sinus tachycardia is classified as adequate or inadequate.

Inadequate sinus tachycardia persists at rest and does not depend on stress and medication. Accompanied by sensations of a strong heartbeat and lack of air.

Symptoms of sinus tachycardia

Manifestations of sinus tachycardia depend on the degree of its severity, duration and nature of the underlying disease, which entailed a change in heart rate.

With sinus tachycardia, patients may complain of palpitations, discomfort, a feeling of heaviness or pain in the region of the heart.

Also, the condition may be accompanied by shortness of breath and weakness, frequent dizziness, increased fatigue and decreased performance, insomnia and worsening mood.

With sinus tachycardia, there is a gradual onset and end of the attack. With prolonged tachycardia, there is a decrease in blood pressure and a cold snap of the extremities.

Diagnosis of sinus tachycardia

In a comprehensive examination of a patient with suspected sinus tachycardia, a number of examinations are carried out, including to identify the cause of a heart rhythm disorder.

The survey plan includes:

ECG for determining the frequency and rhythm of heart contractions
Holter monitoring allows you to assess changes in heart activity under conditions of normal patient activity
Echocardiography and MRI of the heart are performed to determine intracardiac pathology – the cause of tachycardia
Electrophysiological study allows to determine the mechanism of tachycardia and cardiac conduction disorders
Additionally, a general blood test, determination of the content of thyroid-stimulating hormones in the blood, electroencephalography of the brain and others may be required.

What You Can Do

Self-medication is unacceptable, you must consult a doctor. And also exclude factors that contribute to an increase in heart rate: strong tea, coffee, alcohol, cigarettes, spicy foods and chocolate. If possible, you should protect yourself from psycho-emotional and physical overload.

Treatment

What a doctor can do

Treatment is primarily aimed at eliminating the root cause of sinus tachycardia, that is, the underlying disease.The main specialist is a cardiologist, but he may need additional consultations from a neurologist, endocrinologist and other doctors.

A patient with sinus tachycardia may be prescribed sedatives, β-blockers, calcium antagonists, and other drugs.

In the absence of the effect of conservative therapy, transvenous RFA of the heart can be prescribed, that is, restoration of normal heart rhythm by cauterizing the affected area of the heart. In severe cases, implantation of an artificial pacemaker (pacemaker), an artificial pacemaker, may be recommended.