Вы находитесь на странице: 1из 6

Austin Van Niel

Advanced Writing
Dr. Suzanne Richard

Alternative Treatments to Supraventricular Tachycardia


Supraventricular tachycardia (SVT) is the most common type of cardiac arrhythmia

across all demographics. It is characterized by a spontaneous and rapid increase in heart rate
that cannot be explained by exertion and can possibly have spontaneous remission. It is a
medical emergency that if left untreated has two possible outcomes. Either a spontaneous
conversion to normal sinus rhythm or ventricular fibrillation leading to asystole. The first line
treatment after the onset of symptoms that are unresponsive to vagal maneuvers has always
been a drug called adenosine (Ceresnak et al.). Adenosine functions by having a negative effect
on atrioventricular node conduction thereby slowing the heart rate. However, adenosine only
has a half life of approximately one minute, and oftentimes the patient will re-enter SVT once it
has been metabolized therefore is not feasible for management until the underlying cause is
rectified (Rankin et al.). There is very little agreement in the medical community as to where to
proceed from this point pharmacologically, surgically, or to electrically rectify the symptoms with
synchronised cardioversion because there are limitations in staffing as well as a direct result of
contraindications. This literature review will examine the current treatments and proposed
alternative treatments, as well as contraindications in the pediatric and adult populations.

For the sake of simplicity patients with chronic illness or congenital heart disease have
been excluded from discussion. Wolff-Parkinson-White Syndrome has too much conduction
variability and does not respond well to pharmacotherapy. Congenital heart disease has a
different causality than SVT since the tachycardia or other conduction error is caused by leaky
valves and septal defects that cause oxygenated and deoxygenated blood to combine and
induce hypoxia. The hypoxia induces the release of catecholamines which will increase the
heart rate dramatically, but is not the result of a conduction error that adenosine or any of the
drugs discussed will alleviate. Patients with prior histories of cardiac surgery or transplant were
also excluded. Dosages of medications discussed have been included to remove any disparity
from off label dosing due to other conditions or indications.


Under American Heart Association guidelines, all patients presenting with tachycardia
are first treated with vagal maneuvers. These maneuvers are designed to stimulate the vagus
nerve which has acetylcholinergic projections to the cardiac muscle and will slow the heart rate
without the addition of pharmacologic treatment. For many patients this is enough to convert
them back to normal sinus rhythm (NSR). The most commonly used in pediatric patients is to
induce the diving reflex by placing ice bilaterally on the cheeks (Lewis et al.). In the adult
population, the valsalva maneuver is used where the patient tries to exhale forcefully into an
occluded syringe. In either population, rectal stimulation by inserting a rectal thermometer probe
has been shown effective (Delacretaz).

Since vagal maneuvers alone have been shown to only be effective 48% of the time
(including spontaneous conversion to NSR) (Lewis et al.) the next step is to use adenosine.
Adenosine is an endogenous purine nucleoside that is rapidly metabolized but acts long enough
to have an antiarrhythmic effect without the side effects of long term usage. It works by blocking
the atrioventricular node which is responsible for the initiation of cardiac activity. This has been
demonstrated and proven to have an 80-100% efficacy in 600 cases with a mean of 93%, this
figure includes arrhythmias induced in electrophysiologic studies (Rankin et al.). The
recommended starting dose for adults is a 6mg (Delacretaz) intravenous bolus for adult patients
while in pediatric patients the recommended dosage is 0.1mg/kg (Lewis et al.).

SVT is an umbrella term that includes many subtypes of arrhythmias. Broadly, it is

defined as a tachycardic rhythm that electrically originates above the ventricles, typically in the
atrioventricular node which is why adenosine is so effective at stopping this rhythm. Atrial
fibrillation is the most common SVT in the adult population but is very rare in the pediatric
population (Rajkumar et al.). Atrial flutter and multifocal atrial tachycardia typically affect patients
who are over the age of fifty. Paroxysmal SVT includes wide and narrow complex QRS and can
affect patients of all ages. Sinus tachycardia typically presents in patients greater than 10 years
of age and occurs more frequently in females than in males. With paroxysmal SVT and sinus
tachycardia there is no underlying physical abnormality, and these most frequently have re-
entrant pathways that are resistant to adenosine treatment (Delacretaz).

The re-entry mechanism is what causes the SVT to relapse once the short lived
adenosine wears off. Here, a cardiac muscle bundle erroneously connects the atria to the
ventricles creating a new conduction pathway that causes a preexcitation that causes
contraction of the atria and the ventricles to be synchronous and on EKG will show that the
retrograde P wave is buried in the QRS complex. The rapid onset and termination are also key
to the diagnosis of SVT as it demonstrates this rapid re-entry mechanism differentially
diagnosing it from a panic disorder (Delacretaz). These mechanisms are exacerbated by
excessive caffeine intake (Nagajothi et. al), alcohol, stress, and/or illicit drugs, which may also
make the SVT more drug resistant (Ceresnak et al.).

Current First Line Treatment:

When presented with a patient in SVT where the valsalva or other vagal maneuvers
were unsuccessful, as was the first dose of adenosine, it is common practice to try another dose
of adenosine. In pediatric patients, it is seen that a dosage at double the concentration is given
(0.2mg/kg) and in one case of the study set triple the concentration (0.3mg/kg). This was met
with limited success as only 50% of patients responded to the repeated dose of adenosine even
three or four times. Patients in the study over thirteen years of age were given an adult dosage
of 6mg IV bolus to a 38% success rate after a second dose at 12mg. These patients who were
not refractory were given other antiarrhythmic drugs once admitted to the intensive care unit but
with great variety (Lewis et al.). Adult patients are treated with 6mg IV bolus to a similar success
rate as the pediatric population and a second dose of 12mg IV bolus is about 40% effective

While adenosine is widely and successfully used to convert SVT to NSR, there are a lot
of side effects that patients will experience with repeated doses. The most common side effect
is chest pain or pressure not associated with previous cardiac pain. This may be worse in
patients who suffer from angina pectoris at baseline from stimulation of adenosine sensitive pain
receptors. Patients with asthma can experience bronchospasm and constriction especially when
inhaled but this effect appears to be reduced by bolus injection. There is one reported case in
the literature of an asthmatic suffering from a bronchospasm directly after bolus injection but this
is widely accepted as an anomaly. Hypotension from the resultant vasodilation is not typically
seen because of the endogenous reflexive sympathetic discharge during a bolus injection.
Careful monitoring is highly indicated in patients who are receiving an adenosine infusion or
who are under anesthesia (Rankin et al.). These side effects are usually helped by the fact that
adenosine has such a short half life and symptoms resulting from adenosine resolve in several
minutes (Link). This is especially evident when transient asystole, heart block, bradycardia, and
ventricular standstill caused by adenosine resolve without intervention after several seconds
(Rankin et al.).

Second Line Pharmacological Treatment:

There are many options at this point if the SVT has not converted to NSR with
adenosine and fluids because now an atrioventricular conduction issue has most likely been
ruled out. Most importantly the SVT must be deemed narrow QRS complex to proceed with
pharmacologic intervention (Wettersten et al.). Much of the community suggests verapamil at a
5mg bolus every 5 minutes up to 15mg. Verapamil is a class-IV antiarrhythmic agent calcium
channel blocker. It works by slowing the conduction of electricity in the sinoatrial and
atrioventricular nodes. There is a high concentration of calcium channels in these regions and
verapamil will decrease the impulse conduction through these nodes (Delacretaz).Verapamil
also has the effect of slowing the release of catecholamines in the periphery which arguably can
better control the arrhythmia as it stops noradrenaline release (Wettersten et al.). It will also
have the added effect of dilating blood vessels in the periphery and is therefore contraindicated
in patients who are not hemodynamically stable or in pediatric patients whose blood pressure is
far below an adult level at baseline (Lewis et al.). Verapamil should be avoided in patients where
a left ventricular abnormality is suspected as the effects may induce ventricular fibrillation as the
electrical output of the atrioventricular node may no longer be sufficient to fully contract the left
ventricle where there is already decreased output (Setaro et al.).

Diltiazem dosed at 0.25 mg/kg of body weight over a 2-min period with a maintenance
infusion of 5-15 mg/hr, is another class-IV antiarrhythmic drug that works similarly to verapamil.
It is a calcium channel blocker with the same mechanism as verapamil but also causes coronary
vasodilation (Link). Although it would appear as though diltiazem has less hypotensive effects
than verapamil (Phillips et al.), neither of these drugs were used to treat any of the pediatric
patients in any of the studies published in The Journal of Pediatrics due to the risk of causing
hypotension in patients who already have low blood pressure. Verapamil however has more
long term applications as it is more bioavailable orally than diltiazem and can be used
prophylactically to prevent further arrhythmia in a home care setting (Wettersten et al.).

Third Line Pharmacological Treatment:

After this point in caring for a patient who is unresponsive to diltiazem or verapamil there
are even more options because now the care is moving to off label uses for drugs, and drugs
with a lot of contraindications from the massive amount of side effects. Some of the literature
argues that this is the point where the patient can be deemed unstable and the only course of
treatment is a synchronised cardioversion. Others assert that if the patient can be deemed
hemodynamically stable then the pharmacologic treatments can continue. There is no literature
to support the claim that either one of these is more successful, but in separate studies they
were shown to have an equal efficacy although these studies used different exclusion criteria for
their sample data.

Digoxin was a drug used in all pediatric patients in the literature, mostly in the ICU due to
the intense monitoring that is required at a dosage of 8-12g/kg. It does not however cause any
vasodilation because it works by reversing the sodium-calcium exchanger in the myocardium
lengthening phase 4 of cardiac contraction reducing heart rate. It was not used or suggested in
adult patients because it has severely toxic interactions with verapamil (Moj et al.).
Procainamide is used in both the pediatric and adult population once the emergent tachycardia
has stopped since it does not have the negative side effects of adenosine. This is infused at
30mg/min up to 17mg/kg. These both have a very long half life of greater than twenty-four hours
so it is important to monitor the patient and to check for signs of toxicity.

Esmolol was only mentioned briefly as the dosage is very complicated and has a short
half life which makes it a big time sink on the nursing staff but the dosage is a 0.5mg/kg bolus
followed by 0.05-0.2mg/kg/min infusion for 4 minutes, then repeat bolus, then infuse at
0.1mg/kg/min, if a third bolus is required infuse at 0.15mg/kg/min to a max of 80mg or 1mg/kg
whichever comes sooner (Delacretaz).

Nonpharmacologic Treatment and Conclusion:

It has been suggested that in order to spend less time waiting to see if drugs can work it
is best to simply use synchronized cardioversion to try and reset the heart back into rhythm
should the first and second lines of pharmacotherapy does not work. This is indicated in all
cases of wide QRS complex SVT (Link) and in cases of narrow complex SVT where there was
no temporary remission from pharmacotherapy (Delacretaz).
Synchronized cardioversion has been found to be more effective in pediatric patients
and patients with poor venous access. Since the half life of most of the drugs given for SVT is
so short, a complete dose may not make it all the way to the myocardium before it is
metabolized (Lewis et al.). The inherent risks of cardioversion are outweighed by the risks of
waiting for spontaneous conversion as SVT can lead instead to spontaneous ventricular
fibrillation. Statistically it was found to be equally as effective as alternative agents for converting
to NSR but with none of the side effects and with significantly less time needed for conversion.
Sedation may or may not be used for cardioversion depending on patient preference or

Vagal maneuvers alone are more than likely going to convert the patient back to NSR
from SVT. If not then one round of adenosine is the most likely candidate that will cause the
patient to convert back to NSR. After this there are more options open to care providers
depending on the specifics of the case, how stable the patient is, whether or not they can wait to
figure out what is going to work best for them, or how long the patient is going to be compliant
with potentially more lengthy care in their level of discomfort.There are however long lists of side
effects and contraindications with all of these medications. A synchronised cardioversion may be
the best course of treatment when the first or second line drugs do not work at converting to or
sustaining NSR as it is just at effective as these second and third line drugs without any of the
side effects and especially when the patient is borderline wide QRS complex SVT. Synchronized
cardioversion is indicated first in all cases of wide QRS complex SVT. What the patient will
tolerate best in their condition needs to be solved on a case to case basis that takes into
consideration the pros and cons of each treatment and what the patient is willing to do.

Ceresnak, Scott R. MD. et al. (2013). Lone Atrial Fibrillation in the Young Perhaps Not So
Lone?. The Journal of Pediatrics , Volume 162 , Issue 4 , 827 - 831.

Delacretaz, Etienne M.D. (2006). Supraventricular Tachycardia. The New England Journal of
Medicine, 354:1039-51.

Lewis, Jonathan MD. et al. (2017). Acute Management of Refractory and Unstable Pediatric
Supraventricular Tachycardia. The Journal of Pediatrics, Volume 181 , 177 - 182.e2.

Link, Mark S. MD., (2012) Evaluation and Initial Treatment of Supraventricular Tachycardia.The
New England Journal of Medicine, 367:1438-1448.

Moj D, et al. (2017). Clarithromycin, Midazolam, and Digoxin: Application of PBPK Modeling to
Gain New Insights into Drug-Drug Interactions and Co-medication Regimens. AAPS J.
298-312. doi: 10.1208/s12248-016-0009-9.

Nagajothi, Nagapradeep MD. et al. (2008). Energy Drink-related Supraventricular Tachycardia.

The American Journal of Medicine, Volume 121 , Issue 4 , e3 - e4.

Phillips, BG. et al. (1997). Comparison of intravenous diltiazem and verapamil for the acute
treatment of atrial fibrillation and atrial flutter. Pharmacotherapy. 17(6):1238-45.

Rajkumar, Christopher A. MD. et al. (2017). Adenosine induced ventricular fibrillation in a

structurally normal heart: a case report.Journal of Medical Case Reports, 11:21 DOI

Rankin, Andrew C. MD. et al. (1992). Adenosine and the Treatment of Supraventricular

Setaro, John F. et al. (1990). Usefulness of verapamil for congestive heart failure associated
with abnormal left ventricular diastolic filling and normal left ventricular systolic
performance. The American Journal of Cardiology. Volume 66, Issue 12, 1990, Pages

Wettersten, Nicholas MD. et al. (2015). Not Simply Sinus Tachycardia. The American Journal of
Medicine, Volume 128 , Issue 9 , e13 - e14.