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|Classification and external resources|
|Classification and external resources|
Supraventricular tachycardia (SVT) is a condition presenting as a rapid heart rhythm originating at or above the atrioventricular node. Supraventricular tachycardias can be contrasted with the potentially more dangerous ventricular tachycardias—rapid rhythms that originate within the ventricular tissue.
Although "SVT" can be due to any supraventricular cause, the term is most often used to refer to a specific example, paroxysmal supraventricular tachycardia (PSVT), two common types being atrioventricular reciprocating tachycardia and AV nodal reentrant tachycardia. In the older adult population atrial fibrillation becomes a common type of supraventricular arrhythmias—though it is typically considered separately. In general, SVT is not life-threatening, though it may cause worsening heart function if prolonged.
In general, SVT is caused by one of two mechanisms: The first is re-entry; the second is automaticity. Re-entry (such as AV nodal reentrant tachycardia and atrioventricular reciprocating tachycardia) often presents with an almost immediate onset with sudden increase in heart rate. A person experiencing this type of PSVT may feel the heart rate accelerate from 60 to 200 beats per minute or more. Typically, when it reverts to normal rhythm, this is also sudden.
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 a only proportion of the fast impulses to pass through to the ventricles. In a condition called 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.
In automatic types of SVT (atrial tachycardia, junctional ectopic tachycardia), there is more typically a gradual increase and decrease in the heart rate. These are due to an area in the heart that generates its own electrical signal.
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:
atrioventricular origin (junctional tachycardia):
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:
Individual subtypes of SVT can usually be distinguished by the electrical characteristics of the electrocardiogram (ECG).
Most supraventricular tachycardias 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. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin.
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 how it is spread.
SVTs can be separated into two groups, based on whether they involve the AV node for impulse maintenance or not. Those that do so can be terminated by slowing conduction through the AV node. Those that do not will not usually be terminated by AV nodal blocking maneuvers. In these circumstances, transient AV block is still useful, as temporary slowing will often unmask the underlying rhythm abnormality.
AV nodal blocking can be achieved in at least three different ways:
A number of physical maneuvers increase 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 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 and try to exhale forcibly as if straining during a bowel movement. Holding the nose and exhaling against the obstruction has a similar effect.
There are other vagal maneuvers including: holding one's breath for a few seconds, coughing, plunging the face into cold water, (via the diving reflex), 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.
Reducing coffee, alcohol, or tobacco use or increasing the amount of rest may help to alleviate symptoms. Pressing down gently on the top of closed eyes may also bring heartbeat back to normal rhythm for some people suffering from atrial or supraventricular tachycardia (SVT).
Adenosine, an ultra-short-acting AV nodal blocking agent, is indicated if vagal maneuvers are not effective. If successful, followup therapy with diltiazem, verapamil or metoprolol may be indicated. Adenosine may be safely used during pregnancy.
If the patient is unstable or other treatments have not been effective, synchronized electrical cardioversion may be used.
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.
There is a newer treatment for SVT involving the AV node directly. This treatment is called Cryoablation. 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. With Cryoablation, a supercooled catheter is used (cooled by nitrous oxide gas), and the tissue is frozen 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.
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. Tony Blair, former PM of the UK, was also operated on for atrial flutter. Anastacia was diagnosed with the disease. 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. 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.
Movie/Animation of SVT: Video section: The University of Iowa Children's Hospital