Supraventricular Tachycardia

Episodes of fast heartbeat can last for few minutes to 1 to 2 days until the condition gets treated. Increased heartbeat of more than 150 – 279 beats/minutes causes poor cardiac output, which in turn gives rise to the following signs and symptoms [7]:

• Shortness of breath
• Dizziness
• Palpitations
• Chest pain with dyspnea
• Nausea
• Diaphoresis
• Syncope

Infants, who have developed SVT, showcase poor feeding habits, lethargy, and loss of interest in feeding and shallow breathing.

• A preliminary physical examination will be done to determine the heart rate. Physical examination would also reveal a forceful pulse rate in the neck. Heart rate in individuals with SVT would be above 100 – 250 beats/minute. Children would have a higher heart beat and would also show signs of poor blood circulation. 
• Conducting electrocardiography (ECG) is important for diagnosing SVT. If this test is carried out during an episode of SVT, then appropriate diagnosis can be made and other causes of rapid heartbeat can also be ruled out [8].
• In addition to ECG, more specialized tests such as electrophysiology to diagnose the exact location in the heart that is triggering SVT would also be necessary. Imaging studies such as chest radiography, transthoracic echocardiography and MRI of heart are also indicated in diagnosing other associated conditions such as pulmonary edema, congenital heart disease and cardiomegaly [9].

The following methods are involved in the treatment of supraventricular tachycardia:

• Physical maneuvers: This is the method of choice when the atrioventricular node is involved in the causation of SVT. Physical maneuvers work by increasing the intra thoracic pressure which in turn affects the pressure sensor in the arch of the aorta. The valsavar maneuver should be primarily tried in order to end the episode of SVT. In this, the individuals are asked to hold their breath and simultaneously exhale forcibly similar to the process of bowel straining.
• Medications: Medications such as adenosine, is indicated if physical maneuvers does not bring about any positive effect [10]. 
• Cardioversion: Electrocardioversion is used in cases when other treatment methods did not bring about any desired effect. It is one of the most effective modes for restoring sinus rhythm.

In majority of cases, prognosis of the condition mainly depends on the underlying heart disease. Individuals with SVT having a structurally normal heart, have an excellent prognosis. In cases, when SVT occurs due to Wolff-Parkinson-White syndrome, there is a certain percentage of sudden death due to development of atrial fibrillation [6].

Patients with paroxysmal SVT are at an increase risk of developing heart failure, myocardial ischemia and pulmonary edema. Individuals, who do not have any congenital heart defect and are suffering from SVT, are at least risk of sudden death.

SVT has many causes among which the noted cause is Wolff-Parkinson-White syndrome which can be inherited. It can be caused by other underlying diseases like chronic obstructive pulmonary disease (COPD) or heart failure. Prolonged intake of medicines like digoxin or theophylline, and heart surgery can also predispose to the development of the condition.

Anatomically, the heart has a total of 4 chambers, constituting of 2 atria and 2 ventricles. A heartbeat occurs as a result of electrical signal that is produced by the sinoatrial node. These electrical signals spread across the muscles of the heart causing it to contract, thereby producing a “beat”. Any disturbance in this pathway causes abnormal electrical signals to be transmitted to heart, and this gives rise to the condition known as supraventricular tachycardia. Tachycardia means fast heartbeat and supraventricualr means the region above the ventricles. Therefore, fast heartbeat that originates within the ventricles is termed as supraventricualr tachycardia [2]. 

Paroxysmal SVT occurs in about 1 – 3 cases per 1000 individuals. In other words, it has a prevalence rate of 0.2%. Of the several types, atrial fibrillation is the most common type affecting approximately 3 million individuals of US. Statistics have revealed that, by the year 2050, atrial fibrillation will affect more than 7.5 million people.
The incidence of Wolff-Parkinson-White syndrome is estimated to occur in about 3 out of every 1000 individuals [3] [4].

There are two mechanisms that trigger the onset of SVT; re-entry and automaticity. In the re-entry mode, individuals experience a sudden increase in the heartbeats; which is characterized by about 150 – 200 beats per minute. In the automaticity mode, there is a gradual increase in heartbeat. Such a type of condition occurs majorly due to generation of the heart’s own electrical signal.

Supraventricular tachycardia can also occur as a result of abnormal electrical activity in the heart due to congenital defect; a condition known as Wolff-Parkinson-White syndrome. In this syndrome, there is a “bypass tract” that bypasses the atrioventricular node, which in turn results in transmission of the fast heartbeat directly to the ventricles. This creates several loops of overlapping signals which predisposes an individual to develop SVT [5].

There is no way to prevent the onset of SVT. However, to prevent the recurrence of SVT in the future, medications such as verapamil and beta-blockers are used. These drugs along with anti-arrhythmics can also be given for preventing recurrence of SVT episodes.

Supraventricular tachycardia (SVT) is a potentially life threatening condition, demanding immediate medical attention. SVT often refers to paroxysmal supraventricular tachycardia which is an episodic disorder with an abrupt onset and termination. Medications and other therapies help in controlling the occurrence of SVT [1].

• Definition: Supraventricular tachycardia is a condition wherein there is rapid heartbeat of more than 150 – 200 beats/min that originates from above the ventricles. This occurs due to improper electrical activity in the heart which causes development of SVT.
• Cause: Abnormal electrical activity in the heart causes SVT. If infants have congenital defect in the structure of the heart, it is a favorable sign for the development of SVT. In addition, other factors such as excessive consumption of alcohol and caffeine, smoking and use of illicit drugs can also trigger episodes of SVT.
• Symptoms: Symptoms of SVT include shortness of breath, palpitations, anxiety, and development of discomfort in the chest, rapid pulse rate and dizziness. In severe cases, individuals can also faint due to SVT.
• Diagnosis: A preliminary physical examination to determine the heart rate will be done. Following this, electrocardiogram will also be carried out. Imaging studies such as chest radiography, cardiac MRI and transthoracic echocardiography are also indicated in diagnosis of SVT.
• Treatment: Physical maneuvers are the preliminary line of treatment for SVT. If these don’t work then medications and cardioversion techniques may have to be employed.

1. Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995; 332:162.
2. Montoya PT, Brugada P, Smeets J, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. Eur Heart J. Feb 1991;12(2):144-50.
3. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. Jan 1998;31(1):150-7. 
4. Chugh SS, Havmoeller R, Narayanan K, et al. Worldwide epidemiology of atrial fibrillation: a Global Burden of Disease 2010 Study. Circulation 2014; 129:837.
5. Trohman RG. Supraventricular tachycardia: implications for the intensivist. Crit Care Med. Oct 2000;28(10 Suppl):N129-35.
6. Benjamin EJ, Wolf PA, D'Agostino RB, et al. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 1998; 98:946.
7. Wood KA, Drew BJ, Scheinman MM. Frequency of disabling symptoms in supraventricular tachycardia. Am J Cardiol. Jan 15 1997;79(2):145-9.
8. Farre J, Wellens HJ. The value of the electrocardiogram in diagnosing site of origin and mechanism of supraventricular tachycardia. In: Wellens HJJ, Kulbetus HE, eds. What's New in Electrocardiography. The Hague, Belgium; Martinus Nijhoff; 1981:131-71.
9. Xie B, Thakur RK, Shah CP, Hoon VK. Clinical differentiation of narrow QRS complex tachycardias. Emerg Med Clin North Am. May 1998;16(2):295-330. 
10. Camm AJ, Garratt CJ. Adenosine and supraventricular tachycardia. N Engl J Med 1991; 325:1621.

• P wave inversion
  User33213, 2018-10-06 20:06