Supraventricular tachycardia 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, 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 caused by one of two mechanisms: The first is re-entry; the second is automaticity.
Re-entry 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 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 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, 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.
Types
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 Atrial origin:
Ectopic atrial tachycardia Multifocal atrial tachycardia
Atrial fibrillation with rapid ventricular response
Atrial flutter with rapid ventricular response (Without rapid ventricular response, fibrillation
and flutter are usually not classified as SVT)
Atrioventricular origin: AV nodal reentrant tachycardia or junctional
reciprocating tachycardia Permanent junctional reciprocating tachycardia,
a form of JRT that occurs predominantly in infants and children but can occasionally
occur in adults
AV reciprocating tachycardia – visible or concealed
Junctional ectopic tachycardia Signs and symptoms
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:
Pounding heart Shortness of breath
Chest pain Rapid breathing
Dizziness Loss of consciousness
For infants and toddlers, symptoms of heart arrhythmias such as SVT are more difficult
to assess since infants cannot communicate these symptoms to others. Caregivers should
watch for lack of interest in feeding, shallow breathing, and lethargy. These symptoms can
be very understated and may be accompanied by vomiting and/or a decrease in responsiveness.
Diagnosis
Individual subtypes of SVT can usually be distinguished by the electrical characteristics
of the electrocardiogram. Most supraventricular tachycardias have a
narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce
a wide QRS complex that may mimic ventricular tachycardia. In the clinical setting, the
distinction between narrow and wide complex tachycardia 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.
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. In general, it is not
considered SVT. Sinoatrial node reentrant tachycardia is caused
by a reentry circuit localised to the SA node, resulting in a P-wave of normal shape and
size that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically
from sinus tachycardia unless the sudden onset is observed. It may sometimes be distinguished
by its prompt response to vagal manoeuvres. Ectopic atrial tachycardia arises from an
independent focus within the atria, distinguished by a consistent P-wave of abnormal morphology
that falls before a narrow, regular QRS complex. It is caused by automaticity, which means
that some cardiac muscle cells, which have the primordial 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 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 is not, by itself, a tachycardia, but meets the definition 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 at such a fast rate, and
so the P:QRS ratio is usually 2:1 or 4:1 pattern,. Because the ratio of P to QRS is usually consistent,
A-flutter is often regular in comparison to its irregular counterpart, A-fib. 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 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, within the AV node. Because the node is immediately
between the atria and ventricle, the re-entry circuit often stimulates both, meaning that
a retrogradely conducted P-wave is buried within or occurs just after the regular, narrow
QRS complexes. Atrioventricular reciprocating tachycardia,
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
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 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.
Treatment 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 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.
AV nodal blocking can be achieved in at least three ways:
Physical maneuvers 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 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. Lying on your back with your legs vertical
and relaxing with slow steady breaths may end the episode.
There are other vagal maneuvers including: holding one's breath for a few seconds, coughing,
plunging the face into cold water,, 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. Medications
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.
SVT that does not involve the AV node may respond to other anti-arrhythmic drugs such
as sotalol or amiodarone. Cardioversion
If the patient is unstable or other treatments have not been effective, synchronized electrical
cardioversion may be used. Prevention
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 incidence of injuring the AV node, requiring a permanent pacemaker.
With Cryoablation, a supercooled catheter is used, 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, 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
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. See also
Tachycardia AV nodal reentrant tachycardia
Inappropriate sinus tachycardia Ashman phenomenon
Junctional rhythm Wolff-Parkinson-White syndrome
References
External links Cardiac Disorders – Open Directory Project
Supraventricular Tachycardia information from Seattle Children's Hospital Heart Center
Movie/Animation of SVT: Video section: The University of Iowa Children's Hospital