Potential Dangers of the Valsalva Maneuver and
Adenosine in Paroxysmal Supraventricular
Tachycardia – Beware Preexcitation
R. NAGAPPAN*, S. ARORA*, C. WINTER†
*Intensive Care Unit & †Emergency Department, Latrobe Regional Hospital, Traralgon, VICTORIA
ABSTRACT
Paroxysmal supraventricular tachycardia (PSVT) is a common clinical problem. Valsalva maneuver
and adenosine are effective therapies for many patients with PSVT, although any conversion to an
irregular or wide complex tachycardia should prompt consideration of a preexcitation syndrome.
We report a case where the Valsalva maneuver and adenosine, in a patient with PSVT and previously
undiagnosed Wolff-Parkinson-White syndrome, caused atrial fibrillation and led to a haemodynamically
unstable wide complex tachycardia and ventricular fibrillation. In PSVT, where preexcitation has not been
excluded, the Valsalva maneuver and adenosine can be potentially dangerous. (Critical Care and
Resuscitation 2002; 4: 107-111)
Key words: Paroxysmal supraventricular tachycardia, Wolff-Parkinson-White syndrome, Valsalva,
adenosine, wide complex tachycardia
Supraventricular tachycardias (SVTs) are a relatively common cardiac dysrhythmia,1 with 40 % being
paroxysmal supraventricular tachycardia (PSVT) caused
by an atrioventricular (AV) nodal reentrant mechanism.2
The Valsalva maneuver enhances vagal tone and can
terminate AV reentrant tachycardias in 80% of cases,
although rarely it may cause atrial dyssynchrony.
Adenosine produces an acute inhibition of AV nodal
function rendering it a suitable agent for treating AV
nodal reentrant tachycardias. However, adenosine can
be harmful in patients who have an irregular tachycardia. For example, if it is administered to patients with
atrial fibrillation who have AV preexcitation, it can
cause ventricular fibrillation.
We report a case of PSVT in a patient with
previously undiagnosed Wolff-Parkinson-White (WPW)
syndrome who developed serious haemodynamic instability following Valsalva maneuver and adenosine.
After reversion to sinus rhythm, an underlying preexcitation (WPW) syndrome was evident.
CASE REPORT
A 25-year-old woman presented to the emergency
department with headache, nausea and chest pain. She
had been in good health previously with no past history
of hypertension, diabetes or cardiac disease. An
electrocardiogram (ECG) had not been performed prior
to her admission.
On examination she was not distressed but
complained of precordial discomfort that radiated down
her left arm. Her pulse rate was 168 beats per minute
and blood pressure was 128/78 mmHg. An ECG
performed at this stage revealed a narrow complex
tachycardia (Figure 1). As a therapeutic measure she
was asked to perform the Valsalva maneuver. The ECG
recorded post-Valsalva revealed an irregular rhythm (i.e.
atrial fibrillation) with a mixture of broad and narrow
QRS complexes (Figure 2).
As this was associated with a worsening of her chest
pain, 6 mg of intravenous adenosine was administered
which only aggravated her chest pain. Her blood
Correspondence to: Dr. R. Nagappan, Intensive Care Unit, Monash Medical Centre, Clayton, Victoria 3168 (e-mail:
ramesh@bigpond.net.au)
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R. NAGAPPAN, ET AL
Critical Care and Resuscitation 2002; 4: 107-111
Figure 1. The 12-lead ECG on presentation showing a supraventricular tachycardia with a ventricular rate of 166 beats per minute.
Figure 2. The ECG post-Valsalva showing a mixture of narrow and broad complex tachycardias.
pressure at this stage was 126/96 mmHg. An ECG after
the intravenous adenosine (Figure 3) was similar to that
following the Valsalva maneuver, although the QRS
complexes appeared to be wider. Her clinical condition
then deteriorated rapidly as she developed an episode of
rapid wide complex tachycardia due to atrial fibrillation
with antegrade conduction through the by-pass tract
(Figure 4). While the defibrillator was being prepared, a
300 mg bolus of intravenous amiodarone was given.
This was followed by an episode of pulseless wide
complex tachycardia and immediately a 300 J direct
108
current shock was given. She became unconscious and
was rapidly intubated and ventilated. She then
developed ventricular fibrillation and a further four
direct current 360 J shocks were used to revert her to
stable sinus rhythm. Following this her pulse returned,
she regained consciousness and was finally extubated.
The post-resuscitation ECG revealed the characteristic
features of Wolff-Parkinson-White (WPW) syndrome
(Figure 5). She was commenced on flecainide 50 mg
twice daily and her remaining course in the intensive
care unit was brief and uneventful.
Critical Care and Resuscitation 2002; 4: 107-111
R. NAGAPPAN, ET AL
Figure 3. The ECG post-adenosine showing a wide complex tachycardia.
Figure 4. The ECG following clinical deterioration showing an episode of rapid irregular wide complex tachycardia.
An echocardiogram revealed a fractional shortening
of 29 % (normal > 26 %) and a structurally normal
heart. A subsequent electrophysiology study confirmed
WPW syndrome with a para septal atrioventricular
accessory pathway. The accessory pathway was managed successfully with radiofrequency ablation. She has
since remained well and asymptomatic.
DISCUSSION
Supraventricular tachycardias affect more than 1 %
of the population, making them a relatively common
clinical problem.1 Approximately 60 % of are due to an
atrioventricular nodal reentrant tachycardia (AVNRT).
The second most common form of paroxysmal PSVT is
AV reentrant tachycardia (AVRT) using an accessory
pathway.2 The term WPW syndrome is applied to
patients with both preexcitation on the ECG and paroxysmal tachycardias.3-4 The AV bypass tract conducts in
an antegrade direction producing, in sinus rhythm, a
typical ECG pattern of a short PR interval (< 0.12 s), a
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Critical Care and Resuscitation 2002; 4: 107-111
Figure 5. The ECG following cardioversion showing the typical features of Wolff-Parkinson-White syndrome.
slurred upstroke of the QRS complex (delta wave) and a
wide QRS complex (Figure 5). In 95% of WPW patients
with PSVT, the reentrant impulse is conducted
antegradely through the AV node and retrogradely
through the bypass tract (orthodromic AVRT).1 In the
other 5% of WPW patients the reverse is true with
antegrade conduction through the bypass tract and
retrograde conduction through the AV node (antidromic
AVRT).3-4 The latter also predisposes to ventricular
fibrillation during atrial flutter or atrial fibrillation.
The Valsalva maneuver, is a voluntary expiratory
effort against a closed glottis. This increases the intrathoracic pressure, intra-abdominal pressure, blood
pressure and, due to the resultant increase in vascular
baroreceptor stimulation, the vagal tone. The increase in
vagal tone often terminates AV nodal reentrant tachycardias and many orthodromic AVRT’s. Adenosine is an
endogenous nucleoside that produces acute inhibition of
sinus node and AV nodal function. This profound but
short-lived effect also makes adenosine suitable for
treating AVNRT’s and many orthodromic AVRT’s.5
However, in wide-complex tachycardias, not caused by
an AV nodal reentrant mechanism with aberrancy,6 it
can be hazardous.
Our patient had been previously asymptomatic until
she presented with a narrow complex tachycardia.
Following the Valsalva maneuver she developed an
irregular rhythm with a mixture of broad and narrow
complexes (Figure 2). The wide complexes at the
beginning and end of the strip were irregular with a peak
rate of 300/min, a prolonged episode is also shown in
Figure 4. While it is often confused with VT, in our case
it was due to AF with a rapid and aberrant ventricular
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response caused by an AV bypass tract. Atrial
fibrillation in the absence of an accessory pathway has a
maximum ventricular response of approximately 220
beats per minute due to the intrinsic properties of the
AV node.
It is not uncommon for patients in PSVT to change
spontaneously to atrial fibrillation. The occurrence of an
irregular tachycardia after the Valsalva maneuver in our
patient, was either a coincidence or due to the Valsalva
maneuver. Possibly the Valsalva maneuver increased the
vagal tone increasing the AV block and therefore
promoted the conduction of the irregular atrial rhythm
through the accessory pathway causing a wide complex
tachycardia (Figures 2, 3 and 4). This has been reported
previously in a patient with AVRT and WPW syndrome.7 Keidar et al,8 also reported a patient in whom
swallowing (i.e. a vagotonic process) induced atrial
tachycardia and fibrillation in a patient with WPW
syndrome.
The presenting ECG did not show any evidence of
preexcitation (Figure 1). The attempt to convert the SVT
to sinus rhythm by the use of a Valsalva maneuver was
standard clinical practice. However, the subsequent use
of adenosine resulted in haemodynamic instability, an
irregular tachycardia, persistence of the tachycardia
(Figure 3) and finally worsening of the dysrhythmia
(Figure 4). The role of adenosine in the management of
haemodynamically stable wide complex tachycardia has
been reported previously.9-11
Adenosine’s proarrhythmic tendency is well described.12-14 In a prospective analysis of 200 consecutive
patients with PSVT undergoing an electrophysiological
examination, adenosine terminated the PSVT in 99% of
Critical Care and Resuscitation 2002; 4: 107-111
patients but caused atrial fibrillation in 12%.15 In our
patient, the dysrhythmia degenerated into a rapid irregular wide complex tachycardia and ventricular fibrillation. The Valsalva maneuver and adenosine blocked
AV nodal conduction and thus aided conduction down
the previously unknown accessory pathway.
The Valsalva maneuver and adenosine are effective
in many cases of PSVT. They are usually successful in
AV nodal reentrant tachycardia (i.e. where an antegrade
slowly conducting limb and a retrograde rapidly
conducting limb exist within the AV node) and in AV
reentrant tachycardia with a concealed accessory pathway (i.e. where the accessory pathway only conducts
retrogradely). In the preexcitation (WPW) syndrome,
the accessory pathway may conduct the impulse in both
directions and in 5 % of cases it is exclusively antegrade.3
Our case illustrates the potential danger of the
Valsalva maneuver in PSVT where the WPW syndrome
has not been excluded and highlights the consequences
of adenosine in the presence of an irregular tachycardia.
While adenosine has a short half-life and a relatively
safe risk profile it should not reduce the application of
clinical skills in the diagnosis of tachyarrhythmias
particularly as adenosine is only beneficial in the
minority of cases of wide complex tachycardias.
The clinician should suspect preexcitation whenever
a narrow complex tachycardia changes in to a wide
complex tachycardia, especially when it is irregular. The
potential for the Valsalva maneuver to precipitate atrial
dyssynchronisation should also be recognised.
Acknowledgments
The authors wish to thank Dr Jack Krafschek,
Monash Medical Centre, Melbourne for electrophysiological confirmation and radiofrequency ablation.
Received: 27 December 2001
Accepted: 25 January 2002
R. NAGAPPAN, ET AL
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