Paroxysmal supraventricular tachycardia

From Wikipedia, the free encyclopedia
Paroxysmal supraventricular tachycardia
supraventricular tachycardia, paroxysmal atrial tachycardia (PAT)[1]
Lead II electrocardiogram strip showing PSVT with a heart rate of about 180.
Classification and external resources
Specialty Cardiology
ICD-10 I47.1
ICD-9-CM 427.0
MeSH D013617

Paroxysmal supraventricular tachycardia (PSVT) is a type of supraventricular tachycardia.[2] Often people have no symptoms.[1] Otherwise symptoms may include palpitations, feeling lightheaded, sweating, shortness of breath, and chest pain.[3] Episodes start and end suddenly.[4]

The cause is not known. Risk factors include alcohol, caffeine, nicotine, psychological stress, and Wolff-Parkinson-White syndrome which often is inherited from a person's parents. The underlying mechanism typically involves an accessory pathway that results in re-entry. Diagnosis is typically by an electrocardiogram (ECG) which shows narrow QRS complexes and a fast heart rhythm typically between 150 and 240 beats per minute.[4]

Vagal maneuvers, such as the valsalva maneuver, are often used as the initial treatment. If not effective and the person has a normal blood pressure the medication adenosine may be tried. If adenosine is not effective a calcium channel blockers or beta blocker maybe used. Otherwise synchronized cardioversion is the treatment.[5] Future episodes can be prevented by catheter ablation.[4]

About 2.3 per 1000 people have paroxysmal supraventricular tachycardia.[6] Problems typically begin in those 12 to 45 years old.[4][6] Women are more often affected than men. Outcomes in those who otherwise have a normal heart are generally good.[4] An ultrasound of the heart may be done to rule out underlying heart problems.[1]



Signs and symptoms[edit]

Symptoms may include palpitations, feeling faint, sweating, shortness of breath, and chest pain.[3] Episodes start and end suddenly.[4]



AV nodal blocking can be achieved in at least three ways:

Physical maneuvers[edit]

A number of physical maneuvers increase the resistance of the AV node to transmit impulses (AV nodal block), principally through activation of the parasympathetic nervous system, conducted to the heart by the vagus nerve. These manipulations are collectively referred to as vagal maneuvers.

The valsalva maneuver should be the first vagal maneuver tried[7] and works by increasing intra-thoracic pressure and affecting baroreceptors (pressure sensors) within the arch of the aorta. It is carried out by asking the patient to hold his/her breath while trying to exhale forcibly as if straining during a bowel movement. Holding the nose and exhaling against the obstruction has a similar effect.[8]

There are other vagal maneuvers including: holding one's breath for a few seconds, coughing, plunging the face into cold water,[8] (via the diving reflex[9]), drinking a glass of ice cold water, and standing on one's head. Carotid sinus massage, carried out by firmly pressing the bulb at the top of one of the carotid arteries in the neck, is effective but is often not recommended in the elderly due to the potential risk of stroke in those with atherosclerotic plaque in the carotid arteries.

Pressing down gently on the top of closed eyes may also bring heartbeat back to normal rhythm for some people with atrial or supraventricular tachycardia (SVT).[10]


Termination of PSVT following adenosine administration

Adenosine, an ultra-short-acting AV nodal blocking agent, is indicated if vagal maneuvers are not effective.[11] If unsuccessful or the PSVT recurs diltiazem or verapamil are recommended.[5] Adenosine may be safely used during pregnancy.[12]

SVT that does not involve the AV node may respond to other anti-arrhythmic drugs such as sotalol or amiodarone.


If the person is hemodynamically unstable or other treatments have not been effective, synchronized electrical cardioversion may be used. In children this is often done with a dose of 0.5 to 1 J/Kg.[13]

Supraventricular tachycardia - Wikipedia, the free encyclopedia

Supraventricular tachycardia

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Supraventricular tachycardia
supraventricular arrhythmia
Lead II electrocardiogram strip showing PSVT with a heart rate of about 180.
Classification and external resources
Specialty Cardiology
ICD-10 I47.1
ICD-9-CM 427.89, 427.0
MeSH D013617

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in upper part of the heart.[1] There are four main types: atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff-Parkinson-White syndrome.[1]

Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.[2]

They start from either the atria or atrioventricular node.[1] They are generally due to one of two mechanisms: re-entry or increased automaticity.[3] The other type of fast heart rhythm are ventricular arrhythmias—rapid rhythms that start within the ventricle.[1] Diagnosis is typically by electrocardiogram (ECG), holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes such as hyperthyroidism or electrolyte abnormalities.[4]

Specific treatments depend on the type of SVT. They can include medications, medical procedures, or surgery. Vagal maneuvers or a procedure known as catheter ablation may be effective in certain types. For atrial fibrillation calcium channel blockers or beta blockers may be used.

Long term some people benefit from blood thinners such as aspirin or warfarin.[5]

Atrial fibrillation affects about 25 per 1000 people,[6]

paroxysmal supraventricular tachycardia 2.3 per 1000,[7] Wolff-Parkinson-White syndrome 2 per 1000,[8] and atrial flutter 0.8 per 1000.[9]



Signs and symptoms[edit]

Signs and symptoms can arise suddenly and may resolve without treatment. Stress, exercise, and emotion can all result in a normal or physiological increase in heart rate, but can also, more rarely, precipitate SVT. Episodes can last from a few minutes to one or two days, sometimes persisting until treated. The rapid heart rate reduces the opportunity for the "pump" to fill between beats decreasing cardiac output and as a consequence blood pressure. The following symptoms are typical with a rate of 150–270 or more beats per minute:

For infants and toddlers, symptoms of heart arrhythmias such as SVT are more difficult to assess because of limited ability to communicate. Caregivers should watch for lack of interest in feeding, shallow breathing, and lethargy. These symptoms may be subtle and may be accompanied by vomiting and/or a decrease in responsiveness.[10]


Holter monitor-Imaging with start (red arrow) and end (blue arrow) of a SV-tachycardia with a pulse frequency of about 128/min.
A 12-lead ECG showing paroxysmal supraventricular tachycardia at about 180 beats per minute.

Subtypes of SVT can usually be distinguished by their electrocardiogram (ECG) characteristics

Most have a narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce a wide QRS complex that may mimic ventricular tachycardia (VT). In the clinical setting, the distinction between narrow and wide complex tachycardia (supraventricular vs. ventricular) is fundamental since they are treated differently. In addition, ventricular tachycardia can quickly degenerate to ventricular fibrillation and death and merits different consideration.

In the less common situation in which a wide-complex tachycardia may actually be supraventricular, a number of algorithms have been devised to assist in distinguishing between them.[11] In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin.

  • Sinus tachycardia is physiologic or "appropriate" when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is identical to a normal sinus rhythm except for its faster rate (>100 beats per minute in adults). Sinus tachycardia is considered by most sources to be an SVT.
  • Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a P-wave of normal shape and size (morphology) that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically from sinus tachycardia unless the sudden onset is observed (or recorded on a continuous monitoring device). It may sometimes be distinguished by its prompt response to vagal maneuvers.
  • Ectopic (unifocal) atrial tachycardia arises from an independent focus within the atria, distinguished by a consistent P-wave of abnormal shape and/or size that falls before a narrow, regular QRS complex. It is caused by automaticity, which means that some cardiac muscle cells, which have the primordial (primitive, inborn, inherent) ability to generate electrical impulses that is common to all cardiac muscle cells, have established themselves as a 'rhythm center' with a natural rate of electrical discharge that is faster than the normal SA node.
  • Multifocal atrial tachycardia (MAT) is tachycardia arising from at least three ectopic foci within the atria, distinguished by P-waves of at least three different morphologies that all fall before irregular, narrow QRS complexes.
Atrial fibrillation: Red dots show atrial fibrillation activity.
  • Atrial fibrillation meets the definition of SVT when associated with a ventricular response greater than 100 beats per minute. It is characterized as an "irregularly irregular rhythm" both in its atrial and ventricular depolarizations and is distinguished by its fibrillatory atrial waves that, at some point in their chaos, stimulate a response from the ventricles in the form of irregular, narrow QRS complexes.
  • Atrial flutter, is caused by a re-entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute. On the ECG this appears as a line of "sawtooth" waves preceding the QRS complex. The AV node will not usually conduct 300 beats per minute so the P:QRS ratio is usually 2:1 or 4:1 pattern, (though rarely 3:1, and sometimes 1:1 where class IC antiarrhythmic drug are in use). Because the ratio of P to QRS is usually consistent, A-flutter is often regular in comparison to its irregular counterpart, atrial fibrillation. Atrial flutter is also not necessarily a tachycardia unless the AV node permits a ventricular response greater than 100 beats per minute.
  • AV nodal reentrant tachycardia (AVNRT) involves a reentry circuit forming next to, or within, the AV node. The circuit most often involves two tiny pathways one faster than the other. Because the node is immediately between the atria and ventricle, the re-entry circuit often stimulates both, appearing as a backward (retrograde) conducted P-wave buried within or occurring just after the regular, narrow QRS complexes.
  • Atrioventricular reciprocating tachycardia (AVRT), also results from a reentry circuit, although one physically much larger than AVNRT. One portion of the circuit is usually the AV node, and the other, an abnormal accessory pathway (muscular connection) from the atria to the ventricle. Wolff-Parkinson-White syndrome is a relatively common abnormality with an accessory pathway, the bundle of Kent crossing the AV valvular ring.
    • In orthodromic AVRT, atrial impulses are conducted down through the AV node and retrogradely re-enter the atrium via the accessory pathway. A distinguishing characteristic of orthodromic AVRT can therefore be a P-wave that follows each of its regular, narrow QRS complexes, due to retrograde conduction.
    • In antidromic AVRT, atrial impulses are conducted down through the accessory pathway and re-enter the atrium retrogradely via the AV node. Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex in antidromic AVRT is often wider than usual, with a delta wave.
  • Finally, junctional ectopic tachycardia (JET) is a rare tachycardia caused by increased automaticity of the AV node itself initiating frequent heart beats. On the ECG, junctional tachycardia often presents with abnormal morphology P-waves that may fall anywhere in relation to a regular, narrow QRS complex. It is often due to drug toxicity.


Impulse arising in SA node, traversing atria to AV node, then entering ventricle. Rhythm originating at or above AV node constitutes SVT.
Atrial fibrillation: Irregular impulses reaching AV node, only some being transmitted.

The following types of supraventricular tachycardias are more precisely classified by their specific site of origin. While each belongs to the broad classification of SVT, the specific term/diagnosis is preferred when possible:

Sinoatrial origin:

  • Sinoatrial nodal reentrant tachycardia (SNRT)

Atrial origin:

(Without rapid ventricular response, fibrillation and flutter are usually not classified as SVT)

Atrioventricular origin (junctional tachycardia):


The main pumping chamber, the ventricle, is protected (to a certain extent) against excessively high rates arising from the supraventricular areas by a "gating mechanism" at the atrioventricular node, which allows only a proportion of the fast impulses to pass through to the ventricles.

In Wolff-Parkinson-White syndrome, a "bypass tract" avoids this node and its protection and the fast rate may be directly transmitted to the ventricles. This situation has characteristic findings on ECG.


Most SVTs are unpleasant rather than life-threatening, although very fast heart rates can be problematic for those with underlying ischemic heart disease or the elderly.

Episodes require treatment when they occur, but interval therapy may also be used to prevent or reduce recurrence. While some treatment modalities can be applied to all SVTs, there are specific therapies available to treat some sub-types. Effective treatment consequently requires knowledge of how and where the arrhythmia is initiated and its mode of spread.

SVTs can be classified by whether the AV node is involved in maintaining the rhythm. If so, slowing conduction through the AV node will terminate it. If not, AV nodal blocking maneuvers will not work, although transient AV block is still useful as it may unmask an underlying abnormal rhythm.


Once an acute arrhythmia has been terminated, ongoing treatment may be indicated to prevent recurrence. However, those that have an isolated episode, or infrequent and minimally symptomatic episodes, usually do not warrant any treatment other than observation.

In general, patients with more frequent or disabling symptoms warrant some form of prevention. A variety of drugs including simple AV nodal blocking agents such as beta-blockers and verapamil, as well as anti-arrhythmics may be used, usually with good effect, although the risks of these therapies need to be weighed against potential benefits.

Radiofrequency ablation has revolutionized the treatment of tachycardia caused by a re-entrant pathway. This is a low-risk procedure that uses a catheter inside the heart to deliver radio frequency energy to locate and destroy the abnormal electrical pathways. Ablation has been shown to be highly effective: around 90% in the case of AVNRT. Similar high rates of success are achieved with AVRT and typical atrial flutter.

Cryoablation is a newer treatment for SVT involving the AV node directly. SVT involving the AV node is often a contraindication for using radiofrequency ablation due to the small (1%) incidence of injuring the AV node, requiring a permanent pacemaker. Cryoablation uses a catheter supercooled by nitrous oxide gas freezing the tissue to −10 °C. This provides the same result as radiofrequency ablation but does not carry the same risk. If you freeze the tissue and then realize you are in a dangerous spot, you can halt freezing the tissue and allow the tissue to spontaneously rewarm and the tissue is the same as if you never touched it. If after freezing the tissue to −10 °C you get the desired result, then you freeze the tissue down to a temperature of −73 °C and you permanently ablate the tissue.

This therapy has further improved the treatment options for people with AVNRT (and other SVTs with pathways close to the AV node), widening the application of curative ablation to young patients with relatively mild but still troublesome symptoms who would not have accepted the risk of requiring a pacemaker.

Notable cases[edit]

After being successfully diagnosed and treated, Bobby Julich went on to place third in the 1998 Tour de France and win a Bronze Medal in the 2004 Summer Olympics. Women's Olympic volleyball player Tayyiba Haneef-Park underwent an ablation for SVT just two months before competing in the 2008 Summer Olympics.[12] Tony Blair, former PM of the UK, was also operated on for atrial flutter.

Anastacia was diagnosed with the disease.[13] Women's Olympic gold medalist swimmers, Rebecca Soni and Dana Vollmer have both had heart surgery to correct SVT. In addition, Neville Fields had corrective surgery for SVT in early 2006. Wrestling manager Paul Bearer's heart attack was attributed to SVT, resulting in his death.[14] Nathan Cohen, New Zealand's two-time world champion and Olympic champion rower, was diagnosed with SVT in 2013 when he was 27 years old.[15][16][17]


  1. ^ Jump up to: a b c d "Types of Arrhythmia". NHLBI. July 1, 2011. 
  2. Jump up ^ "What Are the Signs and Symptoms of an Arrhythmia?". NHLBI. July 1, 2011. Retrieved 27 September 2016. 
  3. Jump up ^ Al-Zaiti, SS; Magdic, KS (September 2016). "Paroxysmal Supraventricular Tachycardia: Pathophysiology, Diagnosis, and Management.". Critical care nursing clinics of North America. 28 (3): 309–16. PMID 27484659. 
  4. Jump up ^ "How Are Arrhythmias Diagnosed?". NHLBI. July 1, 2011. 
  5. Jump up ^ "How Are Arrhythmias Treated?". NHLBI. July 1, 2011. Retrieved 27 September 2016. 
  6. Jump up ^ Zoni-Berisso, M; Lercari, F; Carazza, T; Domenicucci, S (2014). "Epidemiology of atrial fibrillation: European perspective.". Clinical epidemiology. 6: 213–20. doi:10.2147/CLEP.S47385. PMID 24966695. 
  7. Jump up ^ Katritsis, Demosthenes G.; Camm, A. John; Gersh, Bernard J. (2016). Clinical Cardiology: Current Practice Guidelines. Oxford University Press. p. 538. ISBN 9780198733324. 
  8. Jump up ^ Ferri, Fred F. (2016). Ferri's Clinical Advisor 2017: 5 Books in 1. Elsevier Health Sciences. p. 1372. ISBN 9780323448383. 
  9. Jump up ^ Bennett, David H. (2012). Bennett's Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment. John Wiley & Sons. p. 49. ISBN 9781118432402. 
  10. Jump up ^ Iyer, V. Ramesh, MD, MRCP. "Supraventricular Tachycardia". Children's Hospital of Philadelphia. Retrieved June 8, 2014. 
  11. Jump up ^ Lau EW, Ng GA (2002). "Comparison of the performance of three diagnostic algorithms for regular broad complex tachycardia in practical application". Pacing and Clinical Electrophysiology. 25 (5): 822–7. doi:10.1046/j.1460-9592.2002.00822.x. PMID 12049375. 
  12. Jump up ^ "USA Volleyball 2008 Olympic Games Press Kit" (PDF). Retrieved 2013-11-02. 
  13. Jump up ^ "Anastacia delays heart surgery". News of the World. 3 Nov 2008. Retrieved 30 Apr 2010.  External link in |publisher= (help)
  14. Jump up ^ "Paul Bearer Cause of Death – Heart Attack". 2013-03-23. Retrieved 2013-11-02. 
  15. Jump up ^ Ian Anderson (27 August 2013). "Rowing | Bad day for New Zealand crews". Retrieved 30 October 2013. 
  16. Jump up ^ "Heart problems force Olympic champion out of world champs". Radio New Zealand. 26 August 2013. Retrieved 30 October 2013. 
  17. Jump up ^ "Heart trouble rules Cohen out of rowing World Champs". TVNZ. 26 August 2013. Retrieved 30 October 2013.  Scott Brady of punk band Brave The Wild ( suffers from this. He had his first attack on April 9, 2012 while golfing and was hospitalized over night. He was diagnosed April 17, 2014 in Hamilton ON after having an attack walking home from dinner on March 16, 2014.

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