Download Inhibition of Premature Ventricular Contractions by Desflurane

CASE REPORT
Inhibition of Premature Ventricular Contractions by Desflurane
Menachem M. Weiner, MD,* Michael Greco, DNP, CRNA,† Wenchi Kevin Tsai, MD,‡
and Alexander J.C. Mittnacht, MD§
T
HE NEED FOR ANESTHESIA support outside the traditional operating room is increasing rapidly1, including a
substantial increase in the number of procedures performed in the
cardiac electrophysiology (EP) laboratory. Currently, no consensus or evidence-based recommendations exist regarding the type
of anesthetic or anesthetic agents and drugs used to best facilitate
radiofrequency (RF) ablation of tachyarrhythmias. Additionally,
little unambiguous data are available on the impact of specific
anesthetics on the success of various procedures performed in
the EP laboratory. Peters et al2 reported the increase of the
defibrillation threshold by adding lidocaine to propofol sedation
to minimize injection pain during internal cardiac defibrillator
placement, which possibly could cause unnecessary revision
of the lead system. The authors present a case of premature
ventricular contraction (PVC) RF ablation in which the use of
desflurane led to the inhibition of the arrhythmia.
CASE REPORT
A 44-year-old, 188-cm, 109-kg man without significant cardiovascular history presented to his electrophysiologist’s office with recurrent
syncope associated with palpitations. Transthoracic echocardiography
showed normal left ventricular function without significant valvular
abnormalities. Subsequent Holter monitoring and treadmill stress test
showed frequent monomorphic PVCs without evidence of reversible
ischemia. The patient was started on metoprolol, but this failed to
control his arrhythmia. Before this intervention, the patient had undergone two EP studies at another institution under conscious sedation
where the earliest activation was mapped to the ventricular outflow tract
region. Radiofrequency ablation in both right ventricular outflow tract
(RVOT) and left ventricular outflow tract (LVOT) had temporarily
suppressed the PVCs, but the arrhythmia returned once RF energy
was turned off, consistent with an intramyocardial focus. Because of
his continued clinical symptoms, the patient was referred for a repeat
ablation.
Preprocedural electrolyte laboratory values were all within normal
limits (sodium 142 mEq/L, potassium 4.1 mEq/L, calcium 8.6 mg/dL,
magnesium 1.8 mg/dL). The patient had taken his regular dose of
metoprolol, 25 mg, on the morning of the procedure.
According to institutional practice for this type of procedure, no
preprocedure anxiolysis with benzodiazepines was administered
because the electrophysiologists at this institution believe that benzodiazepine administration may lead to suppression of the arrhythmia. In
the procedure room, the patient was sedated with propofol titrated to
effect for the vascular access part of the procedure (up to 100 μg/kg/min),
and monitored according to American Society of Anesthesiologists
(ASA) guidelines including end-tidal CO2 measurement. No lidocaine
was added to the propofol at any point during the procedure as an
adjunct to decrease injection pain. Propofol was discontinued once
femoral venous access was obtained and intracardiac catheters had been
placed. Ten minutes after discontinuing the propofol infusion, the
patient was conversant, appropriately following commands, and the
neurologic status was at baseline. The electrocardiogram (ECG)
showed a ventricular bigeminy with the PVC morphology of a left
bundle-branch block with QRS transition in leads V2/V3 with right
superior axis (Fig 1).
Electrophysiologic mapping was performed using an electroanatomic mapping system (CARTO, Biosense-Webster, Diamond Bar,
CA), and the arrhythmogenic focus (earliest activation) was mapped to
the lateral aspect of the RVOT just below the pulmonic valve. Before
commencement of RF ablation, a continuous propofol infusion was
restarted at 100 μg/kg/min to deepen sedation and to prevent patient
movement and discomfort during the ablation. The patient soon
presented with signs of upper airway obstruction and intermittent
coughing, which interfered with the RF ablation procedure. To achieve
an adequate level of sedation allowing for mapping and ablation
without patient movement and to relieve the airway obstruction, general
anesthesia was induced with propofol (150 mg intravenous [IV] bolus)
and fentanyl (100 μg IV bolus). Vecuronium (7 mg IV bolus) was
administered for neuromuscular blockade and endotracheal intubation
performed. General anesthesia was maintained with desflurane (targeted
end-tidal concentration 5%). A few minutes after desflurane was
started, the PVCs completely disappeared and electrical stimulation
failed to reproduce any PVCs (Fig 2). Desflurane was discontinued and
a total intravenous anesthetic technique using a continuous propofol
infusion at a rate of 125 μg/kg/min was initiated. The PVCs returned as
ventricular bigeminy within a few minutes after desflurane had been
discontinued. When PVCs returned, no end-tidal desflurane was
detected in the breathing circuit. There were no significant changes
in vital signs, including arterial blood pressure, heart rate, or arterial
oxygen saturation. Depth of anesthesia monitoring using the BIS
monitor (Aspect Medical Systems, Newton, MA) was also unchanged
from when desflurane was used. As a proof of the theory, desflurane
was again added at an end-tidal concentration of 1% (with titration of
the propofol down to 90 μg/kg/min), which inhibited the arrhythmia. In
accordance with the authors' prior observation, discontinuation of
desflurane (with reinstitution of the original propofol dose) then
From the *Department of Anesthesiology, Icahn School of Medicine
at Mount Sinai, New York, NY; †Department of Anesthesiology, Icahn
School of Medicine at Mount Sinai, New York, NY; ‡Department of
Medicine, Division of Electrophysiology, Icahn School of Medicine at
Mount Sinai, New York, NY; and §Department of Anesthesiology,
Icahn School of Medicine at Mount Sinai, New York, NY.
Address correspondence and reprint requests to Menachem M. Weiner,
MD, Department of Anesthesiology, The Mount Sinai Medical Center, One
Gustave L. Levy Place, Box 1010, New York, NY 10029-6574. E-mail:
[email protected]
© 2014 Elsevier Inc. All rights reserved.
1053-0770/2602-0033$36.00/0
http://dx.doi.org/10.1053/j.jvca.2013.11.004
Key words: desflurane, arrhythmias, premature ventricular contractions (PVCs), electrophysiology procedures, cardiac anesthesia, inhalational anesthetics
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2014: pp ]]]–]]]
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WEINER ET AL
Fig 1. Electrocardiogram tracing showing a ventricular bigeminy
with the premature ventricular contraction: left bundle branch block
morphology with QRS transition in leads V2/V3 with right superior
axis. PR interval 190 msec, heart rate 76 beats/min, QRS 100 msec,
QT 482 msec, QTc (using Bazett’s formula—QT interval divided by
the square root of the preceding RR interval expressed in seconds)
544 msec.
produced the arrhythmia once more. Given the history of failed RF
ablation in both the RVOT and LVOT region, bipolar ablation was
performed in this region with two ablation catheters causing temporary
suppression of the arrhythmia. However, the PVCs returned once the
RF energy was turned off. Given the lack of efficacy of the ablation, the
procedure was terminated with the patient remaining in ventricular
bigeminy. The patient was discharged home on metoprolol.
DISCUSSION
Providing anesthesia care in the EP laboratory requires a
high level of collaboration and planning between the electrophysiologist and anesthesiologist.3 The diversity of cases
performed, the large variety of treatment strategies available,
the patient’s underlying cardiac function and comorbidities,
and procedural requirements, as well as the patient’s expectations all need to be weighed in when deciding what type of
anesthetic and which anesthetic drugs to choose for a specific
procedure. Naturally this will vary between practitioners and
institutions, and no general guidelines or recommendations
have been published. General anesthesia has been associated
with greater procedural success for atrial fibrillation ablations,
presumably because of less patient movement during critical
lesion placement and the long duration of the procedure.4
Ablation procedures for supraventricular tachycardias other
than atrial fibrillation are often performed with light sedation
or monitored anesthesia care (MAC) only. Although complicated scar-related ventricular tachycardia (VT) ablations are
lengthy procedures that typically require general anesthesia,
including invasive hemodynamic monitoring, PVC ablation or
VTs originating in the right or left ventricular outflow tract
usually are performed with minimal or no sedation. In the VT
ablation setting, a thorough understanding of the type of
ventricular arrhythmia is required. Unlike supraventricular
tachyarrhythmias, there are no consistent anatomic conduction
pathways that can be studied and the effects of the various
anesthetics evaluated. Multiple etiologies of VT have been
described. In general, an arrhythmogenic substrate (eg, scar
tissue), modulating, and triggering factors are involved.5
Although the arrhythmogenic substrate cannot be changed by
an anesthetic technique, the interaction of anesthetic agents
with the autonomic nervous system, neuraxial sympathetic
blocks,6,7 as well as sympathetic ganglion blocks,8 all have
been clearly shown to suppress or terminate VT (triggering and
modulating effects). General anesthesia alone, regardless of a
specific drug, with the possible exception of ketamine,9
generally will reduce the sympathetic output and may impair
arrhythmia induction. It is for this reason that despite conflicting data, the apparent consensus among most electrophysiologists remains that deeper sedation and general anesthesia impair
arrhythmia induction and should be avoided if possible.10
Only scarce and often conflicting data are available regarding specific effects of anesthetic drugs on suppressing VTs.
Sevoflurane and isoflurane have been shown to prolong action
potential duration11 and QT interval.12,13 Desflurane has been
shown to prolong QT interval as well.14 On the other hand,
propofol did not exhibit similar effects.15,16 General anesthesia
and sedation with propofol, however, is often used in patients
presenting in VT storm unresponsive to antiarrhythmia treatment to blunt the sympathetic output and help terminate or
control the VT.17,18 Dexmedetomidine has been used to
successfully treat a case of malignant VT in a child, possibly
because of the significant sympatheticolytic properties associated with central α2-receptor stimulation.19 Potent inhalation
anesthetic agents have been widely used during SVT ablation
procedures, apparently with minimal effect on the inducibility
of supraventricular tachyarrhythmias.20 However, in the VT
ablation setting, isoflurane was shown to suppress the ability to
induce VT.21 Desflurane, an ether derivate closely related to
isoflurane, increases sympathetic nervous system activity
independently of a baroreceptor reflex–mediated effect.22 This
sympathetic activation has been postulated to facilitate the
Fig 2. Electrocardiogram tracing showing sinus rhythm without
any premature ventricular contraction after the administration of
desflurane. PR interval 184 msec, heart rate 61 beats/min, QRS 98
msec, QT 464 msec, QTc (using Bazett’s formula—QT interval divided
by the square root of the preceding RR interval expressed in
seconds) 468 msec.
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DESFLURANE-INHIBITED PREMATURE VENTRICULAR CONTRACTIONS
induction of arrhythmias.23,24 In this case report, the authors
describe for the first time, possible evidence that desflurane,
despite its sympathomimetic properties, can suppress arrhythmias of ventricular origin. Future studies may be able to elicit a
possible mechanism for this suppression. Although a number of
other medications were administered to the patient, the
temporal relationship of suppression of the arrhythmia and
the administration of desflurane remains fascinating. Interestingly, the QT interval was shorter when desflurane was used,
unlike what was reported by Yildirim and colleagues.14
Studies on the effect of anesthetic agents on the inducibility
or suppression of arrhythmias during ablation procedures are
needed to further elaborate this observation. Although the
authors cannot be absolutely sure that other factors besides
desflurane did not contribute to the suppression of the
arrhythmia in this patient, the presented case nevertheless
greatly advances knowledge regarding the potential inhibition
properties of desflurane and its effect during an outflow
ventricular tachycardia RF ablation. Furthermore, because the
relationship among sympathetic tone, genetics, and underlying
arrhythmogenic substrate are likely to be different among
patients, studies on the effects of anesthetic gases on these
arrhythmias is likely to yield a large variety of results. Perhaps
a registry of techniques and effects might be of greater value. In
the absence of more specific data, practitioners are encouraged
to tailor anesthesia technique and anesthetic agents to the
individual patient’s response to facilitate tachyarrhythmia RF
ablation. A high level of collaboration and planning between
the electrophysiologist and the anesthesiologist is imperative
for optimal care to be delivered.
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