Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3970_Библиотеки_им_академика_М_И_Перельмана.pdf
ATRIAL FIBRILLATION
95
Friedman H, Weber-Bornstein N, Deboe S, Mancini 17
JGB. Cardiac care unit admission criteria for suspected
acute myocardial infarction in new-onset atrial fi brilla-
tion. Am J Cardiol. 1987;59:866–869.
Flaker GC, Blackshear JL, McBride R, et al. The 18
Stroke Prevention in Atrial Fibrillation Investigators.
Antiarrhythmic drug therapy and cardiac mor-
tality in atrial fi brillation. J Am Coll Cardiol.
1992;20:527–532.
Michael JA, Stiell IG, Agarwal S, et al. Cardioversion of 19
paroxysmal atrial fi brillation in the emergency depart-
ment. Ann Emerg Med. 1999;33:379–387.
Stoddard MF, Dawkins PR, Prince CR, Ammash NM. 20
Left atrial appendage thrombus is not uncommon in
patients with acute atrial fi brillation and a recent ambolic
event: a transesophageal echocardiographic study. J Am
Coll Cardiol. 1995;25:452–459.
Page RL, Tilsch TW, Connolly SJ, et al. Azimilide 21
Supraventricular Arrhythmia Program (ASAP)
Investigators. Asymptomatic or “silent” atrial fi brilla-
tion: frequency in untreated patients and patients receiv-
ing azimilide. Circulation. 2003;107:1141–1145.
Manning WJ, Silvermann DI, Katz SE, et al. Impaired 22
left atrial function after cardioversion: relation to
the duration of atrial fi brillation. J Am Coll Cardiol.
1994;23:1535–1540.
Falcone RA, Morady F. Armstrong WF. Transesophageal 23
echocardiographic evaluation of left atrial append-
age function and spontaneous contrast formation after
chemical or electrical cardioversion of atrial fi brillation.
Am J Cardiol. 1996;78:435–439.
Kinch JW. Davidoff R. Prevention of embolic events after 24
cardioversion of atrial fi brillation: current and evolving
strategies. Arch Intern Med. 1995;155:1353–1360.
Wyse DG, Waldo AL, DiMarco JP, et al. The Atrial 25
Fibrillation Follow-up Investigation of Rhythm
Management (AFFIRM) Investigators. A comparison of
rate control and rhythm control in patients with atrial
fi brillation. N Engl J Med. 2002;347:1825–1833.
Kosinski EJ, Albin JB, Young E, Lewis SM, LeLand OS 26
Jr. Hemodynamic effects of intravenous amiodarone. J
Am Coll Cardiol. 1984;4:565–570.
Onalan O, Crystal E, Daoulah A, et al. Meta-analysis of 27
magnesium therapy for the acute management of rapid
atrial fi brillation. Am J Cardiol. 2007;99:1726–1732.
Siu CW, Lau CP, Lee WL, Lam KF, Tse HF. Intravenous 28
diltiazem is superior to intravenous amiodarone or
digoxin for achieving ventricular rate control in patients
with acute uncomplicated atrial fi brillation. Crit Care
Med. 2009;37:2174–2179.
Demircan C, Cikriklar HI, Engindeniz Z, et al. 29
Comparison of the effectiveness of intraveous dil-
tiazem and metoprolol in the management of rapid
Anticoagulation and Risk Factors in Atrial Fibrillation
(ATRIA) Study. JAMA. 2001;285:2370–2375.
National Collaborating Centre for Chronic Conditions. 5
Atrial fi brillation: national clinical guideline for manage-
ment in primary and secondary care. London, UK: Royal
College of Physicians; 2006.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 6
2006 guidelines for the management of patients with
atrial fi brillation: full text: a report of the American
College of Cardiology/American Heart Association Task
Force on practice guidelines and the European Society of
Cardiology Committee for Practice Guidelines (Writing
Committee to Revise the 2001 guidelines for the man-
agement of patients with atrial fi brillation) developed
in collaboration with the European Heart Rhythm
Association and the Heart Rhythm Society. EuroPACE.
2006;8:651–745.
Nolan JP, Deakin CD, Soar J, et al. European Resuscitation 7
Council Guidelines for Resuscitation 2005. Section 4.
Adult advanced life support. Resuscitation. 2005;67(S1):
S39–S86.
Weigner MJ, Caulfi eld TA, Danias PG, Silverman DI, 8
Manning WJ. Risk for clinical thromboembolism associ-
ated with conversion to sinus rhythm in patients with
atrial fi brillation lasting less than 48 hours. Ann Intern
Med. 1997;126:615–620.
Thornton JR. Atrial fi brillation in healthy non-alco-9
holic people after an alcoholic binge. Lancet. 1984;2:
1013–1015.
Engel TR, Luck JC. Effect of whiskey on atrial vul-10
nerability and “holiday heart.” J Am Coll Cardiol.
1983;1:816–818.
Menz V, Grimm W, Hoffmann J, Maisch B. Alcohol and 11
rhythm disturbance: the holiday heart syndrome. Herz.
1996;21:227–231.
Chung MK, Martin DO, Sprecher D, et al. C-reactive 12
protein elevation in patients with atrial arrhythmias:
infl ammatory mechanisms and persistence of atrial fi bril-
lation. Circulation. 2001;104:2886–2891.
Psychari SN, Apostolou TS, Sinos L, et al. Relation of 13
elevated C-reactive protein and interleukin-6 levels to
left atrial size and duration of episodes in patients with
atrial fi brillation. Am J Cardiol. 2005;95:764–767.
Dai S, Zhang S, Guo YH, et al. C-reactive protein and 14
atrial fi brillation in idiopathic dilated cardiomyopathy.
Clin Cardiol. 2009;32(9):E45–50.
Mihm MJ, Yu F, Carnes CA, et al. Impaired myofi bril-15
lar energetics and oxidative injury during human atrial
fi brillation. Circulation. 2001;104:174–180.
Zimetbaum PJ, Josephson ME, McDonald MJ, et al. 16
Incidence and predictors of myocardial infarction among
patients with atrial fi brillation. J Am Coll Cardiol.
2000;36:1223–1227.
CHAPTER 6
96
results from the National Registry of Atrial Fibrillation.
JAMA. 2001;285:2864–2870.
Dell’Orfano JT, Patel H, Wolbrette DL, Luck JC, 33
Naccarelli GV. Acute treatment of atrial fi brillation:
spontaneous conversion rates and cost of care. Am J
Cardiol. 1999;83:788–790, A10.
Decker WW, Goyal DG, Boie ET, et al. A prospective, 34
randomized trial of an emergency department observa-
tion unit for acute onset atrial fi brillation. Acad Emerg
Med. 2003;10:543–544.
ventricular rate in atrial fi brillation. Emerg Med J. 2005;
22:411–414.
Haft JI, Habbab MA. Treatment of atrial arrhythmias. 30
Effectiveness of verapamil when preceded by calcium
infusion. Arch Intern Med. 1986;146:1085–1089.
Go AS, Hylek EM, Chang Y, et al. Anticoagulation 31
therapy for stroke prevention in atrial fi brillation: how
well do randomized trials translate into clinical practice?
JAMA. 2003;290:2685–2692.
Gage BF, Waterman AD, Shannon W, et al. Validation 32
of clinical classifi cation schemes for predicting stroke:
97
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
7
Superventricular tachycardia
Theodore Chan
Medical Director, Department of Emergency Medicine, University of California,
San Diego Medical Center, Professor of Clinical Medicine, University of California,
San Diego, San Diego, California, USA
Section I: Case presentation
A 28-year-old woman with a history of asthma pre-
sented to the Emergency Department (ED) complain-
ing of shortness of breath and increased wheezing
over the prior several days. Her symptoms worsened
progressively during this time, despite repeated use
of the patient’s albuterol inhaler. On the day of pre-
sentation, she also noted intermittent chest tightness,
lightheadedness, and palpitations particularly when
exerting herself.
In addition to her inhaler, the patient’s only medica-
tion was an oral contraceptive. She denied any recent
travel or preceding illnesses. She did not smoke, and
denied any illegal drug use. The family history was
notable for a cardiac condition in her father, the spe-
cifi cs of which were unknown to the patient.
The triage vital signs included: blood pressure 125/62
mmHg, respiratory rate 22 breaths/min, temperature
37.2°C (98.9°F). The triage nurse noted that the “pulse
rate was too fast to count.” The oxygen saturation was
93% on room air. On initial evaluation, the patient
was a young woman in mild respiratory distress, who
was able to speak only in short sentences. On chest
auscultation, there were diffuse wheezes bilaterally
with a prolonged expiratory phase. The cardiac exam-
ination was notable for a rapid regular tachycardia
with no murmurs, gallops, or rubs. The remainder of
the examination was otherwise unremarkable.
The patient was given oxygen by nasal canula, and
placed on a cardiac monitor. A 12-lead EKG was
obtained demonstrating a rapid, regular narrow QRS
complex tachycardia at a rate of 212 beats/min with
ST depressions in the infero-lateral leads (Figure 7- 1).
There were no prior EKGs available for comparison.
Section II: Case discussion
Dr Peter Rosen: This is an interesting tachydysrhyth-
mia case because there is a confounding disease that
might force us to alter our approach. If this were
simply a patient who developed a tachycardia, and
came in with an EKG like this, I suspect most of us
would reach immediately for pharmacologic therapy.
However, this patient’s symptomatology suggests that
either she’s not tolerating this tachycardia very well,
or her problem is her bronchial airway disease. How
does this change your approach to this patient?
Dr Amal Mattu: The fi rst thing I would do to treat
this patient is to attempt vagal stimulation such as
a Valsalva maneuver, avoiding potential interactions
between medications and her underlying condition. If
this didn’t work, then I would go directly to a cal-
cium channel blocker if the patient’s blood pressure
remains as stable as it is right now. I would avoid ade-
nosine as this may produce worsening bronchospasm
in a patient who is already bronchospastic.
CHAPTER 7
98
PR: What forced you to conclude that this isn’t a sinus
tachycardia caused by hypoxia?
SG: The fi rst thing that is striking is the rate. A ven-
tricular rate of greater than 200 beats/min is not typi-
cal of a sinus tachycardia, which is what you would
expect if the patient were having symptoms that were
related to the asthma alone. Then you must think,
what sort of narrow complex dysrhythmias cause a
heart rate in the 200 beats/min range? There aren’t
too many, besides either an AV nodal reentry (AVRT)
or AV reentry tachycardia (AVNRT).
DB: There are retrograde P waves that you can see
in the inferior leads just after the QRS complex
that further suggest that this is AVRT or AVNRT.
Although there is some overlap between those two
conditions in terms of where the retrograde P waves
show up, the small positive defl ections right after
the QRS complex in II, III, and AVF suggest that
this reentry tachycardia is most likely the less com-
mon AVRT.
PR: Is there an upper limit to sinus tachycardia? What
rate would you use for a cut-off?
AM: The formula generally used to predict maxi-
mum heart rate in stress testing is 220 minus the age.
Assuming the patient is neither abusing cocaine nor
is hyperthyroid, I would think this formula could be
used in this scenario as well.
PR: How effective are vagal maneuvers? All I seem to
get when I use one is patients with cold faces and cold
limbs, and with hearts still beating very rapidly.
Dr Shamai Grossman: Adenosine also counteracts the
effects of theophylline. Formerly, when theophylline
was used more regularly in asthma therapy, if patients
were given adenosine, it sometimes blocked the effects
of the theophylline, and that alone could exacerbate
the patient’s asthma symptoms. Today, we think about
this when patients manifest ischemia during pharma-
cologic stress tests with adenosine, as here, and we
would employ theophylline as the antidote.
PR: I grew up practicing medicine when theophylline
was virtually the only treatment we had for asthma,
and there are still some practitioners who use it. One
of the side effects of theophylline is that it produces
tachycardia that persists long after the reactive airway
disease is still active. The patients on chronic theophyl-
line therapy often walked around with a pulse rate
of 150–180 beats/min. Although this patient denies
taking other medications, I would keep in mind that
patients frequently do not accurately remember which
medications they take.
Dr David Brown: I recall the most characteristic
tachycardia associated with theophylline toxicity as
MAT, multifocal atrial tachycardia.
SG: You might be thinking of the chronic obstructive
pulmonary disease (COPD) patient who takes theo-
phylline, but in general, theophylline is more likely to
cause sinus tachycardia or supraventricular tachycar-
dia (SVT).
PR: Along these lines, I wouldn’t give this patient a beta-
blocker for the supraventricular tachycardia because of
the effect on bronchospasm.
Figure 7.1 Initial 12-lead EKG demonstrating regular, narrow QRS complex tachycardia.
SUPERVENTRICULAR TACHYCARDIA
99
remember she has recently used a beta-agonist, so to
allow this medication to wear off, I would probably
delay electrical cardioversion a bit longer.
PR: What if the paramedics call this case into you,
and say she’s beginning to complain of chest pain. It’s
a rainy night, and it is going to be 30 minutes before
they can bring the patient in.
AM: If she’s still hemodynamically stable, with a nor-
mal mental status and clear lungs, I would still give
diltiazem. The alternative would be to sedate her and
cardiovert her. In terms of safety, diltiazem has such a
good safety profi le, and is so effective that, in a per-
son who is hemodynamically stable, it’s just a matter
of getting to the right dose. However, if she’s starting
to drop her blood pressure, develop heart failure, or a
decreased level of consciousness, then electrical cardio-
version would be my fi rst choice.
PR: What dose would of diltiazem would you start
with?
AM: I usually start with about 15 mg in an average size
person, rather than the weight-based manufacture rec-
ommendation, which usually comes to about 20 mg.
I prefer to start lower, as given its half-life, it will last
for about 45 minutes. If it doesn’t work, I would give
a second dose 5–10 minutes later. Eventually you will
achieve the dose that that will work.
PR: If you gave this patient diltiazem in the fi eld, and
she converted to the second EKG here, would you still
bring her to the ED?
TC: I am unaware of any EMS agencies that would
give a treatment like diltiazem, and not bring her to
an ED. In part this is because the diltiazem will remain
in her system for a while during which she should be
monitored, and in part because the symptoms may
recur. Given her ongoing asthma exacerbation, she
will probably require hospital admission regardless.
PR: Now that you have converted her tachycardia, is
there any interference with your approaches to treat-
ing her asthma fl are-up? Are you afraid that as you
treat her asthma fl are, she might revert right back into
this supraventricular tachycardia?
SG: I believe that if you treat her asthma fl are-up you
will make her less likely to revert back to the SVT.
Although beta-agonists can cause tachycardia, in this
case the asthma likely increased her heart rate in the
AM: It’s diffi cult to know for sure how effective these
maneuvers are. The patients we see represent a very
skewed population because, in most patients in whom
vagal maneuvers work, they convert themselves at
home and never come to the ED. As a result, the vagal
maneuvers we do in the ED often don’t work because
they already failed at home. Nevertheless, although
we have a skewed patient population, when a patient
presents with an SVT, I think it’s still reasonable to
give vagal maneuvers a try.
DB: There was a study about 10 years ago that com-
pared the Valsalva maneuver to carotid sinus mas-
sage for SVT. It did not show signifi cant differences
between the techniques. The study further found
that a quarter of these patients converted with vagal
maneuvers.
1
PR: There are a large number of alternative vagal
maneuvers that have been described, some of which
I would have a hard time getting a patient to allow,
such as a digital rectal examination, or putting a
patient’s face or even one of the limbs in ice water.
One maneuver that I found particularly effective is
to place a MAST suit on the patient. Many patients
would convert because of the blood pressure rise
obtained from infl ating the MAST suit. However, it’s
hard to fi nd a MAST suit anymore.
PR: For how long would you try vagal maneuvers
before starting pharmacotherapy?
DB: I usually start doing vagal maneuvers while the
nurse is drawing up the adenosine or diltiazem. In
other words, I generally do not give vagal maneuvers
more than a few minutes to work.
PR: I almost never do vagal maneuvers anymore;
I just can’t see risking a stroke from a carotid mas-
sage. I think adenosine is safer, and far more effective.
Diltiazem is a good alternative, especially if the dys-
rhythmia turns out to be rapid atrial fi brillation rather
than a supraventricular tachycardia. What would
make you want to electrically cardiovert this patient?
Dr Theodore Chan: In this case, as she is hemody-
namically stable, the blood pressure is adequate, the
mental status is at baseline, and I think the respira-
tory symptoms are more likely related to her asthma,
you have time. In many cases with these types of
tachycardias you do have more time, and no need to
jump to cardioversion. In this case, it’s also useful to
CHAPTER 7
100
medicines or some other sympathomimetic agent.
If it’s a fi rst episode, I would tell the patient to stay
away from those medicines, and ensure follow up. As
long as this is a fi rst, isolated episode that converted
easily, I wouldn’t start outpatient medication. If this
is a recurrent episode where I can’t come up with a
precipitant, and they are not already on medication
for an SVT, then I would probably start a low-dose
beta-blocker if there are no contraindications. I would
not use a beta-blocker for this patient because of the
asthma. Instead, I might start a low-dose calcium
channel blocker, and arrange close follow up with
a primary care physician, or, preferably, with a car-
diologist. Some of my colleagues, however, prefer to
initiate medications even with a fi rst episode, if there
are no obvious precipitants.
TC: Another option, particularly with recurrent epi-
sodes, is to prescribe a calcium channel blocker or
beta-blocker that could be taken only when the patient
senses that she’s having a recurrence of the SVT. This
so-called “pill-in-the-pocket” approach could obviate
the need for long-term prophylactic therapy.
PR: Are we missing subtle cases of Wolff-Parkinson-
White (WPW), or the other congenital accessory tract
diseases if the second EKG looks normal? Is there
some sort of special diagnostic workup that those
patients need to be revealed as having this problem?
SG: If you don’t pick up fi ndings consistent with
WPW on EKG, either on their posttreatment EKG
or on their pretreatment EKG, it is hard to identify
WPW in the ED without the patient telling you that
they have a history of WPW. The only way you may
ultimately know whether this patient has WPW may
be with an event or Holter monitor, or if she ends up
having an electrophysiology (EP) study.
DB: During the EP study, she could be injected with
adenosine when not acutely bronchospastic. This will
poison the AV node for a few seconds, and allow her
to conduct through a bypass track if it actually exists
and is functional. About 70% of reentry tachycardias
are caused by AV nodal reentry tachycardia, where
the electrical circuit is confi ned completely to the AV
node. However, about 30% are related to AV reentry
tachycardia, where the circuit involves a bypass track
with orthodromic conduction around this bypass
track. These patients have WPW with a functioning
bypass track. If these patients go into atrial fi brillation
fi rst place, and if you treat the asthma, her baseline
heart rate will actually decrease. I might emphasize
here that I would discharge patients who have no
other concomitant symptomatology with their SVT
and who remain in a sinus rhythm for at least the
amount of time it takes to check a set of electrolytes,
and ensure that a repeat EKG is normal. Perhaps you
might set the patient up with outpatient monitoring,
but in a patient who doesn’t have a concomitant dis-
ease process or signs of ischemia, hospitalization is
not particularly useful
PR: Are you aware of any reason why steroids would
be contraindicated, or would cause a dysrhythmia
recurrence?
DB: I think that they are indicated here for the treat-
ment of asthma, and I would have no hesitation for
delivering them.
PR: I might hesitate if I thought the patient was in
heart failure, as the steroids could make that a lit-
tle worse, but I don’t think that’s the case here. Do
you think this patient needs an electrophysiology
work-up?
DB: The original tracing showed retrograde P waves
that were no longer visible when the patient converted
to a sinus rhythm. This confi rms that these were retro-
grade P waves, and clinches the diagnosis of a reentry
tachycardia. Given that she has a condition that can
be treated defi nitively with radiofrequency ablation or
some similar technique, I would refer her to an elec-
trophysiologist. This way, she may avoid life-long sup-
pressant therapy such as with beta-blockers, which
cause depression, or antidysrhythmics that have a host
of other side effects. I would also keep in mind that,
at age 28, a recurrent SVT is far better tolerated then
at 70.
PR: Assuming that she has converted successfully to a
sinus rhythm, whether it be through vagal maneuvers
or from pharmacology, are there any medications that
you like to put the patient on to prevent immediate
relapse in the next 48 hours, or are you comfortable
with allowing nature to declare itself?
AM: If this is a fi rst time episode, and the patient is
not currently on medications, I would check the his-
tory for a trigger. Perhaps the patient has been taking
a lot of caffeine lately. I’ve seen chocolate set this off.
Perhaps the patient is taking over-the-counter cold
SUPERVENTRICULAR TACHYCARDIA
101
tachycardia, but the term is generally used to refer
to the three most commonly encountered forms of
paroxysmal, or sudden-onset, SVT, which are atrial
tachycardia, AVNRT and AVRT.
2
Published data on the incidence of SVT in the gen-
eral population varies widely and depends on what
cardiac rhythm disturbances are included in the defi -
nition. When referring to paroxysmal tachydysrhyth-
mias, the prevalence is approximately 2.25 per 1,000.
3
Age and gender may infl uence the prevalence of cer-
tain types of SVTs. AVRT often initially presents at a
younger age (mid-20s) compared with AVNRT (mid
30s).
4
So-called “lone” paroxysmal SVT (not associ-
ated with any cardiac structural disease) is also more
commonly present in younger patients. Paroxysmal
SVT is more commonly diagnosed in women than
men, whereas the opposite is true for atrial fl utter.
4
Paroxysmal SVT can be classifi ed in a number of
different ways. First, these tachydysrhythmias can be
classifi ed by their underlying etiology, as noted above,
as atrial tachycardia, AVNRT, or AVRT. Atrial tachy-
cardias comprise approximately 10% of cases, usu-
ally from an atrial focus origin either due to abnormal
automaticity or triggered activity. A reentry mecha-
nism is more common, with 60% of cases caused by a
reentry circuit located within the AV node (AVNRT),
and the other 30% involving an atrioventricular
reentry circuit mediated by an accessory pathway
(AVRT).
5
SVTs can also be classifi ed by whether the condition
requires AV nodal conduction to maintain the tachy-
dysrhythmia, referred to as AV node-dependent or AV
at some point in the future, they could have hemody-
namic compromise by rapidly conducting down their
bypass tract. This, in my mind, reinforces the need to
refer these patients for an EP study.
Case resolution
Despite the patient’s asthma exacerbation, the
patient underwent cautious treatment in the ED for a
supraventricular tachycardia with intravenous adenos-
ine administration, after which she converted to a sinus
tachycardia at a rate of 128 beats/min (Figure 7-2). She
was also treated for the acute asthma exacerbation
with inhaled nebulized albuterol and systemic steroid
administration. The asthma symptoms did not improve
signifi cantly, perhaps in part due to the administra-
tion of adenosine, and she was subsequently admitted
to the hospital for further treatment and evaluation.
After a two-day hospitalization, during which time the
patient’s asthma exacerbation resolved and she had
no additional episodes of SVT, she was discharged to
home in good condition.
Section III: Concepts
Background/epidemiology
Supraventricular tachycardia (SVT), by defi nition,
includes all forms of tachycardia that involve the atria
or atrioventricular (AV) node for initiation and con-
tinuance. Technically, SVT includes sinus tachycardia,
atrial fi brillation, atrial fl utter, and multifocal atrial
Figure 7.2 Repeat 12-lead EKG following pharmacologic conversion with adenosine. Note the patient is now in a sinus
tachycardia with clear P wave activity in a 1:1 AV pattern.
CHAPTER 7
102
of all ages, and is not usually associated with under-
lying structural heart disease. However, accessory
pathways that can play a role in certain types of
AVRTs are associated with structural heart condi-
tions, such as Ebstein’s anomaly and hypertrophic
cardiomyopathy. Similarly, atrial tachycardias may
be associated with congenital or acquired heart dis-
ease involving the atria. In addition, while SVT is
uncommonly associated with myocardial ischemia,
this possibility should be considered in older patients
who may have a history of underlying coronary ath-
erosclerosis.
2
Finally, an SVT may be the result of an
underlying metabolic disorder, such as hyperthyroid-
ism, or electrolyte abnormalities, and additional his-
tory should focus on determining if these conditions
may be present.
The physical examination should fi rst focus on
the patient’s vital signs and underlying hemody-
namic status. Tachycardia in adults, by defi nition, is
a heart rate greater than or equal to 100 beats/min,
and classic SVTs usually present with rates varying
from 120–220 beats/min. Higher rates may occur,
but these raise concern for other etiologies, includ-
ing ventricular tachycardia or the conduction of an
atrial tachycardia, such as atrial fi brillation, directly
down an accessory pathway. Slower ventricular rates
can also be seen in the presence of an atrial tachydys-
rhythmia where AV block or delay is present, such as
from pharmacologic beta-blockade.
In many cases, the remainder of the physical exami-
nation is often normal, particularly if the patient has
converted to a sinus rhythm by the time of the evalu-
ation.
5
During an episode of SVT, examination of the
neck veins may reveal intermittent prominent jugular
venous A waves from right atrial contractions against
a closed tricuspid valve, the so-called “Frog sign.”
9
The examination should otherwise focus on evidence
of acute cardiac compromise as a result of the dys-
rhythmia, underlying structural heart disease, or
sequelae of possible etiologies (i.e., hyperthyroidism).
Rarely, patients who have persistent or long-standing
tachycardia (weeks to months) may present with evi-
dence of cardiomyopathy and chronic cardiac failure
on examination.
2
Etiologies
As noted above, SVTs are frequently classifi ed as AV
node-independent or node-dependent, which can be
node-independent. This information can be of clinical
utility by indicating whether the SVT can be termi-
nated by AV blocking measures. Finally, paroxysmal
SVTs can be classifi ed by EKG appearance, such as
the duration of the RP interval (long RP tachycardia
or short RP tachycardia).
Initial workup history and physical examination
The initial tasks in the ED for patients with SVT are
to obtain vital signs, determine the patient’s overall
hemodynamic and cardiovascular status, and initi-
ate any immediate stabilization measures as war-
ranted. Patients commonly present with a variety of
complaints and symptoms, including palpitations,
lightheadedness, fatigue, syncope and presyncope,
weakness, chest pain or discomfort, anxiety, short-
ness of breath, diaphoresis, and a pounding sensation
in the neck or chest.
6
Increased urinary frequency
and polyuria, resulting from the diuretic effect of
increased atrial natriuretic factor release in response
to elevated atrial pressures (from contraction against
a closed AV valve), has been reported with SVT as
well.
7
Syncope can be observed in up to 15% of
patients with SVT; this is usually just after the ini-
tiation of the tachydysrhythmia, or as a result of a
long pause following termination of the abnormal
rhythm.
4
In addition, syncope may also occur not
as a direct result of the SVT, but from a vasovagal
response to the dysrhythmia.
8
Classically, patients complain of sudden onset and
occasionally abrupt termination of their symptoms
associated with SVT. This paroxysmal quality can
assist in differentiating SVT from other tachycar-
dias, including sinus tachycardia, which often has a
more gradual onset and termination. However, some
patients may not perceive a sudden onset of their
associated symptoms; similarly, an abrupt termina-
tion may not be obvious, particularly if the patient
converts to a rapid sinus tachycardia as a result of
anxiety-related increased adrenergic drive or hemo-
dynamic compromise associated with the previous
SVT rhythm.
On history, patients should be asked about the
duration and frequency of symptomatic episodes
and any possible triggers. In particular, patients
should be asked about caffeine intake, alcohol con-
sumption, and recreational drug use, which are
known precipitants.
5
An SVT can occur in patients
SUPERVENTRICULAR TACHYCARDIA
103
AVRT has also been associated with certain struc-
tural heart diseases, such as congenital Ebstein’s
anomaly.
AVRT occurs when there is a larger macroreentry
circuit that involves the normal conduction path-
way through AV node and an accessory bypass tract
between the atria and ventricles. Impulses travel from
the atria to the ventricles down one of these pathways,
and then back to the atria up the other pathway, thus
completing the circuit loop.
Orthodromic conduction in an AVRT occurs when
antegrade conduction proceeds from the atria to the
ventricles through the normal conduction system and
AV node, and retrograde conduction takes place from
the ventricles back to the atria through the accessory
bypass tract. Because activation of the ventricles occurs
through the normal conduction pathway (unless
there is a preexisting aberrancy), the QRS complex
is narrow in orthodromic AVRT. In this case, differ-
entiation from AVNRT can be diffi cult. Antidromic
conduction occurs when antegrade conduction from
the atria to the ventricles occurs through the bypass
tract, and retrograde conduction occurs from the
atria to the ventricles through the normal AV node
and conduction system. Because the ventricular acti-
vation occurs via the abnormal bypass tract, the QRS
complex is abnormally wide and can have a bizarre
morphology in antidromic AVRT (Figure 7-3). In this
case, differentiation from ventricular tachycardia or
other tachycardias with aberrant ventricular conduc-
tion can be diffi cult.
Other less common forms of SVT include focal
junctional tachycardia, also known as junctional
ectopic tachycardia, and nonparoxysmal junctional
tachycardia. These rare AV tachydysrhythmias origi-
nate from abnormal automaticity or triggered activity
in the AV node, and are often associated with con-
genital heart disease, presenting in early childhood.
Abnormal junctional tachycardias have also been
associated with digoxin toxicity, cardiac ischemia and
infarction, or following cardiac surgery.
Testing
After the initial physical examination and vital
signs, the EKG is the most important test to obtain
in a patient with suspected SVT. Whenever possible,
it is best to obtain a 12-lead EKG during the SVT,
but doing so should not delay immediate therapy to
helpful in not only determining potential etiologies,
but also in providing guidance as to management.
AV Node-Independent: These forms of SVT are
independent of AV nodal conduction and arise from
a source above the AV node. Most commonly, these
types of atrial tachydysrhythmias are caused by a
small atrial focus with abnormal automaticity or trig-
gered activity (such as can occur with digoxin toxi-
city). Although rare, a microreentry circuit within
the atrial tissue (such as with Sinus Node Reentry
Tachycardia) can occur.
AV node-independent dysrhythmias comprise
approximately 10% of all SVTs. Technically, AV
node-independent SVTs include sinus tachycardia,
atrial fl utter, atrial fi brillation, and multifocal atrial
tachycardia; these are tachycardias that all arise above
the AV node and are independent of AV conduction,
but are generally not included in the general use of
the term SVT.
Clinically, atrial tachydysrhthmias typically have
a regular rhythm and rate, ranging from 100–250
beats/min. Because they are not dependent on the AV
node, blockade or delay has little effect on the tachy-
dysrhythmia. AV blockade can slow the ventricular
response to the SVT, but does not terminate the atrial
tachydysrhythmia.
AV Node-Dependent: The more common forms of
SVTs are AV node-dependent. These tachydysrhyth-
mias arise from a reentry circuit that involves the AV
node. As a result, AV nodal conduction is necessary to
maintain the tachydysrhythmia. Blockade of conduc-
tion at the AV node will, in fact, terminate these types
of SVTs.
AVNRT occurs when there is a small microreen-
try circuit located within or near the AV node, and
it comprises approximately 50–60% of SVTs. The
reentry circuit loop itself is made up of slow and
fast pathways with different refractory periods. The
SVT is triggered when a premature atrial impulse
conducts antegrade to the ventricles down one path-
way, and subsequently conducts retrograde back
to the atria up the other pathway, thus completing
the reentry loop. Because the microreentry circuit is
located within or very near the AV node, there is a
near simultaneous, rapid activation of both the atria
and ventricles.
The other primary form of AV node-dependent
SVT is AVRT, which tends to present at an earlier
age and more frequently in men than AVNRT.
10
CHAPTER 7
104
interval (RP and PR interval durations), onset and
termination of the dysrhythmias if seen electrocardio-
graphically, and presence or absence of preexcitation
on the baseline 12-lead EKG.
Atrial tachycardias typically present as a regular nar-
row QRS complex tachycardia (except in the presence
of aberrant conduction) and have a long RP interval.
11
Atrial tachycardias also most commonly terminate
with a ventricular complex, and not an atrial complex
or P wave as seen on a 12-lead EKG. Atrial tachycar-
dias can be differentiated from sinus tachycardia by
the change in P-wave morphology during sinus and
tachycardic rates.
AVNRT classically presents with a regular narrow
complex tachycardia, but rate-related aberrant or
bundle branch block conduction is common and can
result in a wide complex tachycardia. Usually, P waves
are not discernable, particularly at rapid rates, but in
some cases P waves can be seen superimposed within
the QRS complex as pseudo-R, pseudo-Q, or pseudo-S
waves. These waves, which are not seen during nor-
mal sinus rhythm, can be quite specifi c for AVNRT.
12
AVNRT is typically a short RP tachycardia, though this
again can be diffi cult to determine with rapid tachy-
cardias. In addition, AVNRT is usually initiated by a
terminate the abnormal cardiac rhythm if there is
hemodynamic instability.
4
The approach to the 12-lead EKG demonstrat-
ing an abnormal tachycardic rate should focus on
the regularity of the rhythm and the QRS complex
morphology. An irregular tachycardia may be the
result of atrial fi brillation, atrial fl utter and other
atrial tachycardias with variable block, and MAT.
A regular tachycardia can occur with sinus tachy-
cardia, atrial tachycardias or atrial fl utter (without
variable block), and SVTs, including both AVNRT
and AVRT.
The QRS complex can be prolonged, regardless of
the underlying rate, in the presence of aberrant ven-
tricular conduction, bundle branch block, or preex-
citation (in addition to rhythms arising from ectopic
ventricular foci, such as VT). In fact, rate-related bun-
dle branch block is relatively frequent in patients with
SVT.
2
As noted above, antidromic AVRT results in a
wide QRS complex regular tachycardia that is often
diffi cult to distinguish from VT.
In addition to rate, regularity, and QRS complex
morphology, the other EKG fi ndings that may be of
interest in the setting of SVT include the P-wave mor-
phology, relative position of the P wave in the RR
Figure 7.3
A. Reentry mechanism for orthodromic AVRT. Atrioventricular conduction occurs down the AV node and ventriculoatrial
conduction up the accessory pathway, resulting in a narrow QRS complex tachycardia.
B. Reentry mechanism for antidromic AVRT. Atrioventricular conduction occurs down the accessory pathway and
ventriculoatrial conduction up the AV node, resulting in a wide QRS complex tachycardia.