Full text of DOI:10.1213/00000539-200208000-00013

Accelerated Idioventricular Rhythm Associated with
Desflurane Administration
Emmanuel Marret, MD, Olivier Pruszkowski, MD, Arnaud Deleuze, MD, and
Francis Bonnet, MD
D e´ partement d’Anesth e´ sie R e´ animation, H oˆ pital Tenon, Assistance Publique-Hopitaux de Paris, Paris, France
entricular arrhythmia occurs with halothane ad-
ministration (1), and may be complicated by
ventricular tachycardia, especially in the pres-
rhythm. The arterial blood pressure was 130/70 mm Hg.
Desflurane administration was stopped and AIVR disap-
peared spontaneously within 5 min, at a desflurane end-
tidal concentration of 0.8%. At this time, the ECG was sim-
ilar to the preoperative one (Fig. 1). After discontinuation of
desflurane, the patient showed signs of light anesthesia, and
the arterial blood pressure increased to 160/80 mm Hg, so
desflurane was restarted at 3.2% end-tidal concentration
V
ence of hypoxemia or hypercarbia (2). Sevoflurane and
desflurane are volatile anesthetics used for their rapid
onset and offset of action and cardiovascular stability.
Sevoflurane caused fewer ventricular arrhythmias
than halothane during anesthesia for dental extraction
without N O. AIVR reappeared immediately (Fig. 2). The
2
desflurane was again discontinued, but the AIVR persisted
for 5 min, until the end-tidal desflurane concentration de-
creased to 0%. Anesthesia was continued with a target-
controlled IV infusion of propofol with a target concentra-
tion at 5 ␮g/mL, and 20% N O in O . The patient remained
(
1). Although desflurane does not facilitate ventricular
arrhythmia (3), the induction of anesthesia with des-
flurane can result in sympathetic stimulation, which
may induce cardiac arrhythmias, including ventricu-
lar arrhythmias (4,5). We report a case of accelerated
idioventricular rhythm (AIVR) related to the admin-
istration of desflurane.
2
2
in a stable sinus rhythm during the remainder of the
procedure.
Plasma troponin Ic concentrations measured at the end of
surgery and 24 h later were in the normal range (0.02 ␮g/L).
Plasma sodium, potassium, calcium, and magnesium con-
centrations were also normal. During the following 24-h
period, continuous ECG monitoring showed no cardiac
rhythm disorder. Echocardiography performed 2 days later
showed no evidence of valvular heart disease or any evi-
dence of coronary artery disease.
Case Report
A 69-yr-old woman, weighing 69 kg, was scheduled for
pelvic surgery for urinary incontinence. She had previously
undergone multiple surgical procedures for urinary incon-
tinence with no anesthetic complications. A preoperative
examination revealed no signs or symptoms of cardiovascu-
lar disease. The arterial blood pressure was 126/75 mm Hg.
The preoperative electrocardiogram (ECG) showed a sinus
rhythm at 85 bpm, a QRS duration of 0.06 s, and no ventric-
ular ectopic beats.
Discussion
During anesthesia, ventricular arrhythmias have been
documented in patients with previous cardiac disease,
electrolyte disturbances, or in relation to drugs given
intraoperatively (2). AIVR is characterized by an ec-
topic ventricular rhythm with 3 or more consecutive
ventricular premature beats at a rate faster than ven-
tricular escape but slower than 100 to 125 bpm (6). The
electrophysiologic characteristics of AIVR suggest a
mechanism of abnormal automaticity such as en-
hanced phase 4 depolarization of ventricular muscle
fibers, rather than reentrant arrhythmia. AIVR is usu-
ally well tolerated and no specific antiarrhythmic
treatment is recommended apart from removing the
suspected cause. AIVR often occurs in patients with
acute myocardial infarction, especially when throm-
bolysis results in reperfusion (6). It has also been de-
scribed in association with cocaine abuse (7). In this
setting, the arrhythmia is thought to be caused by the
After premedication with hydroxyzine 100 mg, general
anesthesia was induced with sufentanil 20 ␮g and propofol
00 mg. Cisatracurium 8 mg was given to facilitate intuba-
2
tion of the trachea. The lungs of the patient were ventilated
with N O 50% in O and desflurane. Arterial blood pressure
2
2
was 150/80 mm Hg, heart rate was 60 bpm, end-tidal CO2
was 34 mm Hg, and peripheral SaO by pulse oximetry was
2
1
00%. A few minutes later, at a desflurane end-tidal concen-
tration of 5.4%, episodes of ventricular arrhythmia occurred
with wide QRS complexes indicative of AIVR (ventricular
rhythm at this time was 80 bpm) alternating with sinus
Accepted for publication April 11, 2002.
Address correspondence and reprint requests to Dr. Emmanuel
Marret, D e´ partement d’Anesth e´ sie R e´ animation, H oˆ pital Tenon-4,
rue de la Chine, 75970 Paris Cedex 20, France. Address e-mail to
emmanuel.marret@tnn.ap-hop-paris.fr.
DOI: 10.1213/01.ANE.0000019770.06260.95
©
2002 by the International Anesthesia Research Society
0
003-2999/02
Anesth Analg 2002;95:319–21
319

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20 CASE REPORTS
ANESTH ANALG
002;95:319–21
2
Figure 1. Perioperative electrocardiogram after the first administration of desflurane documents sinus rhythm.
Figure 2. Perioperative electrocardiogram during the rapid desflurane readministration (end-tidal concentration: 3.2%) documenting
accelerated idioventricular rhythm with a ventricular rhythm at 80 bpm. One fusion complex (white star) and three sinusal complexes (black
stars) were recorded.
sympathomimetic effects of cocaine on the heart. Co-
caine blocks the reuptake of norepinephrine at nerve
endings. Subepicardial infusion of norepinephrine has
also been reported to cause reversible ventricular ar-
rhythmia (5). Thus, increased cardiac sympathetic ac-
tivity may precipitate ventricular arrhythmia.
Volatile anesthetics, such as halothane, induce ven-
tricular arrhythmia (1). In the presence of certain in-
haled anesthetics, the dose of sympathomimetic drugs
that will produce cardiac arrhythmia is markedly de-
creased (8). Epinephrine normally increases the rate of
phase 4 depolarization in automatic cells. The inci-
dence of catecholamine-induced dysrhythmias was
most frequent with halothane than other inhaled an-
esthetics (9). The rapid administration of desflurane
up to 1.5 minimum alveolar anesthetic concentration
has been associated with systemic hypertension and
tachycardia (10). This is related to a rapid increase in
sympathetic activity and norepinephrine and epi-
nephrine release (11). In vitro studies have also shown
that desflurane may induce intramyocardial cat-
echolamines release (12,13). Submucosal epinephrine
administration induced premature ventricular con-
tractions in patients given 1.0–1.3 minimum alveolar
anesthetic concentration desflurane (3). Thus, we spec-
ulate that the two desflurane rapid sequences of ad-
ministration were responsible for catecholamines re-
lease and precipitated the AIVR episodes in our
patient. The second episode of AIVR started at a
smaller desflurane end-tidal concentration than the

ANESTH ANALG
002;95:319–21
CASE REPORTS
321
2
5
. Nash MP, Thornton JM, Sears CE, et al. Ventricular activation
during sympathetic imbalance and its computational recon-
struction. J Appl Physiol 2001;90:287–98.
first one. At this time, the patient showed signs of
awakening, which would have increased sympathetic
tone. Propofol and N O, also administered to the pa-
2
6. Denes P, Gillis AM, Pawitan Y, et al. Prevalence, characteristics
and significance of ventricular premature complexes and ven-
tricular tachycardia detected by 24-hour continuous electrocar-
diographic recording in the Cardiac Arrhythmia Suppression
Trial. CAST Investigators. Am J Cardiol 1991;68:887–96.
tient, also increase the incidence of ventricular ar-
rhythmia in response to epinephrine injection, and
they may have contributed to the first AIVR episode
(
14,15). However, no episode of AIVR was noted dur-
7
. Benchimol A, Bartall H, Desser KB. Accelerated ventricular
rhythm and cocaine abuse. Ann Intern Med 1978;88:519–20.
ing the remainder of the surgical procedure, when
anesthesia was maintained with propofol and N O.
8. Katz RL, Epstein RA. The interaction of anesthetic agents and
adrenergic drugs to produce cardiac arrhythmias. Anesthesiol-
ogy 1968;29:763–84.
2
We conclude that a rapid administration of desflu-
rane, resulting in transient hypertension and tachycar-
dia, when a patient has a sympathetic imbalance such
as a period of inadequate anesthesia, may precipitate
ventricular arrhythmias such as AIVR.
9
. Johnston RR, Eger EI II, Wilson C. A comparative interaction of
epinephrine with enflurane, isoflurane, and halothane in man.
Anesth Analg 1976;55:709–12.
10. Ebert TJ, Muzi M. Sympathetic activation with desflurane in
humans. Adv Pharmacol 1994;31:369–78.
1
1. Weiskopf RB, Moore MA, Eger EI II, et al. Rapid increase in
desflurane concentration is associated with greater transient
cardiovascular stimulation than with rapid increase in isoflu-
rane concentration in humans. Anesthesiology 1994;80:1035–45.
2. Hanouz JL, Massetti M, Guesne G, et al. In vitro effects of
desflurane, sevoflurane, isoflurane, and halothane in isolated
human right atria. Anesthesiology 2000;92:116–24.
We thank Dr. Duong for his help in analyzing the data.
1
1
1
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