Reversal of Rocuronium-Induced Neuromuscular
Block with the Novel Drug Sugammadex Is Equally
Effective Under Maintenance Anesthesia with
Propofol or Sevoflurane
Bernard F. Vanacker, MD, PhD*
Karel M. Vermeyen, MD, PhD†
Michel M. R. F. Struys, MD, PhD‡
Henk Rietbergen, MSc§
Eugene Vandermeersch, MD, PhD*
Vera Saldien, MD†
Alain F. Kalmar, MD‡
Martine E. Prins, MSc§
In this study we investigated whether the novel reversal drug, sugammadex, is
equally effective at reversing rocuronium-induced neuromuscular block (NMB) in
patients under propofol or sevoflurane maintenance anesthesia. After receiving
propofol for induction, patients were randomized to propofol (n ? 21) or
sevoflurane (n ? 21). Rocuronium 0.6 mg/kg was administered for tracheal
intubation. NMB was monitored using acceleromyography. At reappearance of the
second twitch of the train-of-four ratio, sugammadex 2.0 mg/kg was administered
by IV bolus. The primary end-point was time from start of sugammadex admin-
istration to recovery of train-of-four ratio to 0.9. Mean recovery time was 1.8 min
after both propofol and sevoflurane anesthesia. The 95% confidence interval for the
difference in recovery time between the 2 groups (–0.5 to ?0.4 min) was well
within the predefined equivalence interval (–1 to ?1 min), indicating that recovery
from NMB was unaffected by maintenance anesthesia. Thirteen patients (propofol
n ? 4; sevoflurane n ? 9) experienced adverse events; these were treatment-related
in 4 patients (propofol n ? 3; sevoflurane n ? 1). There were no treatment-related
serious adverse events and no discontinuations or deaths. No residual paralysis
occurred. The safety profile of sugammadex was somewhat more favorable under
propofol than under sevoflurane anesthesia.
(Anesth Analg 2007;104:563–8)
Once surgery is complete, reversal of the action of
neuromuscular blocking drugs (NMBDs) is often per-
formed to accelerate recovery from neuromuscular
blockade (1). At present, cholinesterase inhibitors (e.g.,
neostigmine) are used to reverse the action of NMBDs.
These drugs are nonselective and facilitate cholinergic
transmission throughout the body. They are only
effective when residual neuromuscular function is
present, and there is currently no reliable method of
reversing profound neuromuscular blockade (2,3).
A novel approach to reversing neuromuscular
blockade is sugammadex (Org 25969; NV, Organon
International, Oss, The Netherlands), a drug-specific
modified ?-cyclodextrin that is a selective relaxant
binding agent (SRBD). Unlike the cholinesterase in-
hibitors, which increase the activity of the cholinergic
system, an SRBD directly prevents the pharmaco-
logic action of the NMBD by decreasing the free
concentration of the drug (3). Sugammadex is the
first SRBD developed for the reversal of neuromus-
cular blockade; it acts by rapidly encapsulating
steroidal NMBDs such as rocuronium or vecuronium
to form a stable complex. The results of several ani-
mal studies have shown that sugammadex reverses
rocuronium-induced neuromuscular blockade in vitro
and in vivo (4–6). In addition, phase I and II trials have
shown that sugammadex is effective and safe at
reversing rocuronium-induced blockade in healthy
volunteers and surgical patients undergoing anesthe-
sia with propofol (7,8).
Propofol and sevoflurane are widely used for the
maintenance of anesthesia. In contrast to propofol,
sevoflurane enhances the effects of some NMBDs, in-
cluding rocuronium (9,10). Xue et al. (11) showed that
sevoflurane can significantly prolong the duration of
action of rocuronium and the time to recovery. These
effects are not seen with either propofol or isoflurane (9).
The present study was designed to compare the
efficacy of sugammadex in reversing rocuronium-
induced block in patients in whom anesthesia was
maintained with propofol or with the volatile anesthetic
sevoflurane and to further investigate the overall safety
profile of sugammadex.
From the *University Hospitals Leuven, KU Leuven, Belgium;
†University Hospital Antwerp, Antwerp, Belgium; ‡Ghent Univer-
sity Hospital, Ghent, Belgium; §NV Organon, Oss, The Netherlands.
Accepted for publication May 23, 2006.
Supported, in part, by NV Organon, Oss, The Netherlands.
Address correspondence and reprint requests to Bernard F.
Vanacker, MD, PhD, Department of Anesthesiology, University
Hospitals Leuven, KU Leuven, Herestraat 49, B-3000 Leuven, Bel-
gium. Address e-mail to firstname.lastname@example.org.
Copyright © 2007 International Anesthesia Research Society
Vol. 104, No. 3, March 2007
This was a randomized, multicenter, safety assessor-
blinded, phase II, parallel-group, comparative trial
conducted at three centers in Belgium. The protocol
was approved by an Independent Ethics Committee at
each participating center, and the trial was conducted
in accordance with the current revision of the Decla-
ration of Helsinki, International Conference on Har-
monisation Guidelines, and Good Clinical Practice.
Patients aged 18 yr or older, with ASA physical
status I–III, scheduled to undergo surgery in the
supine position that was anticipated to last for at least
45 min and required muscle relaxation only for tra-
cheal intubation were eligible for inclusion. All pa-
tients gave written informed consent. Patients were
excluded from the trial if they had any of the follow-
ing: expected difficulties with intubation resulting
from anatomical malformations; known or suspected
neuromuscular disorders and/or significant hepatic
or renal dysfunction; history of malignant hyperther-
mia; known or suspected allergy to muscle relaxants,
narcotics, or any other medication used during gen-
eral anesthesia; or if they were currently receiving
medications known to interfere with NMBDs (e.g.,
anticonvulsants or magnesium [Mg2?]); or had previ-
ously participated in this trial or another clinical trial.
In addition, women of childbearing potential not
using an acceptable method of birth control and those
who were breastfeeding or pregnant were not eligible
for the trial.
Anesthesia was induced with an IV opioid followed
by propofol. Patients were then randomized to receive
maintenance anesthesia with either propofol (?6.0
mg · kg?1· h?1by continuous infusion) or sevoflurane
(target minimum alveolar concentration 1.5, adjusted
for age); in both groups, additional opioid was admin-
istered depending on clinical needs. No nitrous oxide
was used. Patients were manually ventilated by mask
using an oxygen-air mixture until tracheal intubation.
Intubation was then performed at maximal neuromus-
cular block and intermittent positive pressure venti-
lation was started using low flow. Ventilation was
adjusted to maintain normal end-tidal CO2.
Neuromuscular block was monitored and recorded
by acceleromyography (TOF Watch®SX; Organon
International, Oss, The Netherlands) using train-of-
four (TOF) stimulation. The stimulated arm was posi-
tioned on an arm board and kept warm using a
warmed blanket. The area where the electrodes were
to be placed was cleaned and two electrodes were
placed on the ulnar nerve trajectory. The transducer
was fixed with its largest flat side against the thumb.
After induction of anesthesia, stabilization and cali-
bration were performed. During the stabilization pe-
riod, a 5-s 50-Hz tetanic stimulation was followed by
repetitive TOF stimulation (supramaximal) for at least
2 min. After calibration (100%), the TOF Watch®SX
was switched to TOF stimulation every 15 s.
After the stabilization period (at least 5 min), each
patient received a single IV bolus dose of rocuronium
0.6 mg/kg for tracheal intubation. When the second
twitch (T2) of the TOF reappeared, a single IV bolus
dose of sugammadex 2.0 mg/kg was administered.
Anesthesia and neuromuscular monitoring were
maintained at least until the ratio between the fourth
and first twitches (TOF ratio) had recovered to 0.9 and
until the end of surgery (minimum of 30 min after
administration of sugammadex).
The occurrence of residual paralysis was also evalu-
ated. Neuromuscular monitoring for the occurrence of
residual paralysis was to be continued for at least 30
min after the recovery of the TOF ratio to 0.9, after
which the patients could be woken up and tracheally
extubated. Oxygen saturation and breath frequency
were monitored for at least 60 min after the recovery
of the TOF ratio to 0.9.
Adverse events (AEs) were recorded from admin-
istration of sugammadex until the postanesthetic visit
that took place at least 10 h after administration of
sugammadex. Serious AEs (SAEs) were also recorded
at follow-up, 7 days after administration of sugamma-
dex. An SAE was defined as any untoward medical
occurrence that at any dose resulted in death, was
life-threatening, required inpatient hospitalization or
prolongation of existing hospitalization, resulted in
persistent or significant disability/incapacity, or was a
congenital anomaly or birth defect. Patients were
questioned and/or examined to obtain data on AEs.
Arterial blood pressure and heart rate were recorded
at screening, at stable anesthesia, i.e., just before
administration of rocuronium (baseline), at 2, 10, and
30 min after the start of sugammadex administration,
and at the postanesthetic visit.
Twelve-lead electrocardiograms were taken at stable
anesthesia, i.e., before administration of rocuronium
(baseline), and at 2 and 30 min after administration of
sugammadex. The corrected electrocardiographic QT
interval (QTc) was monitored as part of the regular
safety monitoring. The QTc is intended to represent
the QT interval at a standardized heart rate of 60 bpm.
Because of its inverse relationship to heart rate, the QT
interval is routinely transformed (normalized) by
means of various formulae into a heart rate indepen-
dent “corrected” value known as the QTc interval. For
drugs that prolong the QT/QTc interval, the mean
degree of prolongation has been roughly correlated
with the observed risk of clinical proarrhythmic
events. Prolongation of the QTc interval was reported
as a SAE if individual QTc changes were ?60 ms
relative to baseline or absolute QTc values were ?500
Recovery from neuromuscular blockade induced
by rocuronium 0.6 mg/kg was studied in the “per
protocol” (PP) population (i.e., all randomized and
treated patients without any major protocol viola-
tions) and in the “intent-to-treat” (ITT) population
Sugammadex Efficacy During Anesthesia
ANESTHESIA & ANALGESIA
(i.e., all randomized patients who received sugamma-
dex and had at least one efficacy assessment). Safety
data were studied in the safety population (i.e., all
subjects who received sugammadex).
The primary end-point was the time from the start
of administration of sugammadex to recovery of the
TOF ratio to 0.9. Secondary end-points were the time
from the start of administration of sugammadex to
recovery of the TOF ratio to 0.7 and 0.8. The confi-
dence interval (CI) approach was used to demonstrate
equivalence in recovery of the TOF ratios to 0.7, 0.8,
and 0.9 between the 2 treatment groups. Equivalence
was claimed if the 2-sided 95% CI for the difference
between the 2 groups was within the interval ranging
from –1 min to ?1 min. The 95% CI was obtained from
a 2-way analysis of variance model, with treatment
and study center as factors.
A sample size of 42 patients had 80% power to
show equivalence in the time to recovery of the TOF
ratio to 0.9 between the two treatment groups (PP
population), assuming an sd in the recovery times of 1
min, a 15% dropout rate, and Gaussian distributed
In addition to presenting descriptive statistics
(mean, sd, and range values per treatment group) a
figure was prepared showing, for each of the two
treatment groups, the percentage of patients for whom
the TOF ratio was not yet recovered to ?0.9 as a
function of the time from the start of administration of
Baseline data were analyzed using descriptive sta-
tistics. Except for QTc interval data, safety data were
reported in a descriptive manner. QTc interval data
were analyzed using a two-way analysis of variance
model and the paired Student’s t-test. Two-sided
statistical testing was conducted and P values less
than or equal to 0.05 were considered statistically
significant. No adjustments for multiplicity were
A total of 42 patients (ASA physical status I–III)
were enrolled and randomized; 21 in each treatment
group (Table 1). All but one patient were Caucasian.
Patients in the propofol group were, on average, older,
heavier, and taller than those in the sevoflurane
group, and more women were enrolled in the sevoflu-
rane group than in the propofol group. None of these
differences were considered to affect the efficacy anal-
ysis. All 42 patients who received sugammadex com-
pleted the trial and were included in the ITT analysis.
One patient in the sevoflurane group had a major
protocol violation (sugammadex administered too
early, ?2 min before reappearance of T2) and was
excluded from the PP analysis.
Mean recovery time from rocuronium administra-
tion to reappearance of T2was 33.0 min in the propo-
fol group and 51.8 min in the sevoflurane group (P ?
0.002) (Table 2).
The mean time from start of administration of
sugammadex to recovery of the TOF ratio to 0.9 was
Table 1. Baseline Characteristics
ASA class I:II:III
Values are mean (SD) or n. ASA ? American Society of Anesthesiology?
* All patients treated.
(n ? 21)
(n ? 21)
Table 2. Time (min) From Start of Administration of
Rocuronium (0.6 mg/kg) to Reappearance of the Second
Twitch (T2; Per Protocol Population)
(n ? 21)
(n ? 20)
* P ? 0.002 versus propofol (Student’s t-test)?
Table 3. Time (min) From Administration of Sugammadex
(2.0 mg/kg) to Recovery of the Train-of-Four (TOF) Ratio
(Per Protocol Population)
(n ? 21)
1.8 (0.7) [0.9–3.4]*
(n ? 20)
1.8 (0.7) [1.1–4.5]Time to recovery of
TOF ratio to 0.9
Time to recovery of
TOF ratio to 0.8
Time to recovery of
TOF ratio to 0.7
Values are mean (SD) [range]. TOF ? train-of-four.
* Data missing for one patient, n ? 20?
1.5 (0.5) [0.9–2.9]1.5 (0.3) [1.1–2.1]
1.3 (0.5) [0.8–2.4]1.3 (0.3) [0.7–1.9]
Figure 1. Percentage of patients who did not recover (train-
of-four [TOF] ?0.9) as a function of time (min) from the start
of administration of sugammadex (2.0 mg/kg) [per protocol
Vol. 104, No. 2, March 2007
© 2007 International Anesthesia Research Society 565
1.8 min in both the propofol and sevoflurane groups
(PP population) (Table 3). The estimated difference in
the mean time to recovery of the TOF ratio to 0.9
between the two groups was –0.0 min with the
corresponding 95% CI ranging from –0.5 to ?0.4 min,
which was well within the predefined range for equiva-
lent efficacy. Results of the ITT analysis supported those
from the PP population with an estimated difference
between the propofol and sevoflurane groups of 0.0 min
(95% CI: –0.4 to ?0.5 min).
Figure 1 shows the percentage of patients who did
not recover to TOF ?0.9 as a function of time from the
start of administration of sugammadex for the two
treatment groups. Complete recovery was achieved in
?3 min by 19 of 20 patients receiving sevoflurane for
maintenance anesthesia and in 19 of 20 patients receiv-
ing propofol (PP population; data for one patient were
missing in the propofol group).
The mean times from start of administration of
sugammadex to recovery of the TOF ratios to 0.8 and
0.7 were 1.5 and 1.3 min, respectively, in both the
propofol and sevoflurane groups (PP population)
(Table 3). Estimated between-group differences in the
mean times to recovery of the TOF ratios to 0.8 and 0.7
were –0.0 min (95% CI: –0.3 to ?0.3 min) and –0.0 min
(95% CI: –0.3 to ?0.2 min), respectively, again show-
ing equivalent recovery in both treatment groups.
Results from the ITT analysis were similar and also
showed equivalent efficacy.
Two examples of TOF Watch®traces obtained
under propofol and sevoflurane maintenance anesthe-
sia are presented in Figure 2.
No residual paralysis was observed in any of the
patients. Two patients were not monitored for at least
30 min after recovery of the TOF ratio to 0.9. One
patient in the sevoflurane group was monitored for
only 11 min, during which time no residual paralysis
was observed. Data on the second patient, in the
propofol group, were not available as a result of
technical difficulties with the TOF Watch®SX. No
residual paralysis was evident in either patient.
Thirteen patients experienced at least 1 AE, 9 in the
sevoflurane group, and 4 in the propofol group. All
AEs were of mild to moderate intensity, except in one
patient in the sevoflurane group who reported severe
In the sevoflurane group one patient developed
hypotension that was considered drug-related, i.e.,
possibly, probably, or definitely related to sugamma-
dex. In the propofol group, one patient developed
drug-related AEs (bradycardia, nausea, and vomit-
ing), and two patients each developed one drug-
related AE (hiccups and hypotension).
Figure 2. Two examples of recovery from neuromuscular blockade induced by rocuronium 0.6 mg/kg followed by sugammadex
2.0 mg/kg at reappearance of the second twitch (T2) under (A) propofol and (B) sevoflurane maintenance anesthesia.
Sugammadex Efficacy During Anesthesia
ANESTHESIA & ANALGESIA
SAEs due to QTc prolongation were observed in
eight patients in the sevoflurane group. These were
mild and were considered unlikely to be related to
sugammadex. Two of these patients had additional
SAEs that were not considered to be treatment related.
One patient experienced postoperative pain that
started 4 days after sugammadex administration and
continued for 3 days. The patient recovered from the
event, which was judged to be related to surgery. The
second patient had urinary retention 8 days after
sugammadex administration, which was not consid-
ered related to sugammadex. The event was of mod-
erate intensity and lasted for 4 days, after which time
the patient recovered.
Results for the QTc interval are based on the
Fridericia correction (13). Prolongation of the QTc
interval seen in the sevoflurane group was already
evident 2 min after administration of sugammadex
(P ? 0.01 versus baseline) (Table 4). The QTc interval
continued to increase and was significantly longer at
30 min compared with baseline (P ? 0.001) or com-
pared with the value at 2 min (P ? 0.006). Results from
the propofol group echoed these findings to a lesser
degree. In the propofol group, the difference at 30 min
compared with 2 min was not statistically significant
(P ? 0.078), suggesting that QTc prolongation was
already apparent before administration of sugamma-
dex. The difference in QTc prolongation between the 2
treatment groups approached significance at 2 min (P
? 0.053) and was highly significant at 30 min (P ?
Overall, arterial blood pressure and heart rate val-
ues were within the agreed safety ranges. An abnor-
mal value was observed at 2, 10, or 30 min post-dose
for systolic blood pressure and/or diastolic blood
pressure in 7 subjects. None of these were considered
to be an AE. For one patient, a decrease in heart rate
from 62 bpm at baseline to 44 and 45 bpm was
reported at 2 and 10 min post-dose, respectively. This
was not considered clinically relevant, and the heart
rate returned to 53 bpm at the 30-min post-dose
This study demonstrates that sugammadex, 2.0
mg/kg, is equally effective at reversing rocuronium-
induced block, regardless of whether the maintenance
anesthetic regimen is propofol or sevoflurane. The
mean times to recovery of the TOF ratio to 0.9 ob-
served in this trial were comparable to those observed
in other trials: 1.3 minutes (8) and 1.7 minutes (14). The
time to reversal of the TOF ratio to 0.9 was longer in
one patient in the sevoflurane group but was within
the clinically acceptable limits of reversal times.
Unlike propofol, sevoflurane enhances the neuro-
muscular blocking action of rocuronium (9–11). This
was confirmed in our trial, in which the mean time
from the start of administration of rocuronium to the
reappearance of T2was almost 19 minutes longer
under sevoflurane anesthesia compared with propofol
anesthesia. However, the results show that anesthesia
with sevoflurane does not reduce the efficacy of
sugammadex in reversing rocuronium-induced block-
ade. This is consistent with the direct mechanism of
action of sugammadex, which encapsulates steroidal
NMBDs, thus producing block reversal (5). In a study
by Kim et al. (15) on the reversibility of rocuronium-
induced block by neostigmine under propofol and
sevoflurane anesthesia, the results showed that the
recovery time of the TOF ratio to 0.7, 0.8, and 0.9 was
significantly longer under sevoflurane anesthesia than
under propofol anesthesia (P ? 0.0001).
In this trial, sugammadex reversed neuromuscular
block within 3 min of administration in the majority of
patients in both treatment groups. This represents a
substantial improvement versus conventional cho-
linesterase inhibitors, which take much longer. Kim et
al. (15) reported a median recovery time of the TOF
ratio to 0.9, after neostigmine administration, of 7.5
(range, 3.4–11.2) minutes under propofol anesthesia
and 22.6 (range, 8.3–57.4) minutes under sevoflurane
anesthesia. Suzuki et al. (16) reported a mean (sd)
recovery time of the TOF ratio to 0.9, after edropho-
nium administration, of 24.7 (14.3) minutes under
Sugammadex was well tolerated with minimal side
effects with both propofol and sevoflurane. Few AEs
were reported that were considered related to sugam-
madex. All AEs except one were of mild-to-moderate
intensity. The most common AEs were nausea and
QTc prolongation. Eight patients in the sevoflurane
group experienced QTc prolongation that met the
criteria for a SAE. None of these patients had values
placing them at risk of arrhythmia, and the events
Table 4. Changes in the Corrected QT Interval (min) From Pre-Sugammadex (Baseline) Administration (Safety Population)
Mean (sd) change from
Results of the comparison of
sevoflurane versus propofol
( n ? 21)
( n ? 21)
10.9 (–0.2, 21.9)
18.8 (7.8, 29.9)
2 min post-dose
30 min post-dose
CI ? confidence interval.
Note: results using Fridericia’s correction are presented. * P ? 0.05; † P ? 0.01; ‡ P ? 0.001 versus baseline?
Vol. 104, No. 2, March 2007
© 2007 International Anesthesia Research Society 567
were considered unlikely to be related to sugamma- Download full-text
dex. Although this study was not designed to evaluate
the effect of sugammadex on QTc prolongation, the
most likely cause was the anesthetics themselves.
Sevoflurane prolongs the QTc interval (17,18) and
although it is generally accepted that propofol can
reduce an already elongated QTc interval (19,20), it
has also been shown to prolong it (20,21).
A previous phase II study has shown that sugam-
madex is effective and safe at reversing rocuronium-
induced block in surgical patients anesthetized with
propofol (8). The present trial confirms these results
and demonstrates that sugammadex, 2 mg/kg, ad-
ministered at reappearance of T2is safe and equally
effective in rapidly reversing rocuronium-induced
blockade in surgical patients under propofol or
sevoflurane maintenance anesthesia, but with a later
appearance of T2in the sevoflurane group. It is
anticipated that larger studies planned for the future,
evaluating the efficacy and safety of sugammadex in
different patient populations and at different times of
reversal, will more fully elucidate the role of sugam-
madex in the reversal of neuromuscular blockade.
Editorial assistance was provided by Julie Adkins at Prime
Medica during the preparation of this paper,supported by NV
Organon. Responsibility for opinions, conclusions, and inter-
pretation of data lies with the authors.
1. Bevan DR. Monitoring and reversal of neuromuscular block.
Am J Health Syst Pharm. 1999;56(Suppl 1):S10–3.
2. van den Broek L, Proost JH, Wierda JMKH. Early and late
reversibility of rocuronium bromide. Eur J Anaesthesiol. 1994;
11 (Suppl 9):128–32.
3. Zhang M-Q. Drug-specific cyclodextrins: the future of rapid
neuromuscular block reversal? Drugs Future 2003;28:347–54.
4. Adam JM, Bennett J, Bom A, et al. Cyclodextrin-derived host
molecules as reversal agents for the neuromuscular blocker
rocuronium bromide: synthesis and structure-activity relation-
ships. J Med Chem 2002;45:1806–916.
5. Bom A, Bradley M, Cameron K, et al. A novel concept of
reversing neuromuscular block: chemical encapsulation of rocu-
ronium bromide by a cyclodextrin-based synthetic host. Angew
Chem Int Ed 2002;41:265–70.
6. Tarver GJ, Grove SJA, Buchanan K, et al. 2-O-substituted
cyclodextrins as reversal agents for the neuromuscular blocker
rocuronium bromide. Bioorg Med Chem 2002;10:1819–27.
7. Gijsenbergh F, Ramael S, Houwing N, van Iersel T. First human
exposure of Org 25969, a novel agent to reverse the action of
rocuronium bromide. Anesthesiology 2005;103:695–703.
8. Sorgenfrei I, Larsen PB, Norrild K, et al. Reversal of
rocuronium-induced neuromuscular block by the selective re-
laxant binding agent, sugammadex: a dose-finding and safety
study. Anesthesiology 2006;104:667–74.
9. Lowry DW, Mirakhur RK, McCarthy GJ, et al. Neuromuscular
effects of rocuronium during sevoflurane, isoflurane, and intra-
venous anesthesia. Anesth Analg 1998;87:936–40.
10. Wulf H, Ledowski T, Linstedt U, et al. Neuromuscular blocking
effects of rocuronium during desflurane, isoflurane, and sevoflu-
rane anaesthesia. Can J Anaesth 1998;45:526–32.
11. Xue FS, Liao X, Tong SY, et al. Dose-response and time-course of
the effect of rocuronium bromide during sevoflurane anaesthe-
sia. Anaesthesia 1998;53:25–30.
12. United States Department of Health and Human Services, Food
and Drug Administration, Center for Drug Evaluation and
Research (CDER) and Center for Biologics Evaluation 12 and
Research (CBER). Guidance for industry: E14 clinical evaluation
of QT/QTc interval prolongation and proarrhythmic poten-
tial for non-antiarrhythmic drugs. October 2005. Available at:
www.fda.gov/cder/guidance/6922fnl.pdf. Accessed on Febru-
ary 8, 2006.
13. Luo S, Michler K, Johnston P, MacFarlane PW. A comparison of
commonly used QT correction formulae: the effect of heart rate on
the QTc of normal ECGs. J Electrocardiol 2004;37(Suppl):81–90.
14. Suy K, Morias K, Hans P, et al. Fast, effective and safe reversal
of rocuronium and vecuronium-induced moderate neuromus-
cular block by the selective relaxant binding agent Org 25969
[abstract]. Anesthesiology 2005;103:A1119.
15. Kim KS, Cheong MA, Lee HJ, Lee JM. Tactile assessment for the
reversibility of rocuronium-induced neuromuscular blockade
during propofol or sevoflurane anesthesia. Anesth Analg 2004;99:
16. Suzuki T, Lien CA, Belmont MR, et al. Edrophonium effectively
antagonizes neuromuscular block at the laryngeal adductors
induced by rapacuronium, rocuronium and cisatracurium, but
not mivacurium. Can J Anaesth 2003;50:879–85.
17. Paventi S, Santevecchi A, Ranieri R. Effects of sevoflurane
versus propofol on QT interval. Minerva Anestesiol 2001;67:
18. Yildirim H, Adanir T, Atay A, et al. The effects of sevoflurane,
isoflurane and desflurane on QT interval of the ECG. Eur J
19. Kleinsasser A, Loeckinger A, Lindner KH, et al. Reversing
sevoflurane-associated Q-Tc prolongation by changing to
propofol. Anaesthesia 2001;56:248–50.
20. Saarnivaara L, Klemola UM, Lindgren L, et al. QT interval of the
ECG, heart rate and arterial pressure using propofol, metho-
hexital or midazolam for induction of anaesthesia. Acta Anaes-
thesiol Scand 1990;34:276–81.
21. Saarnivaara L, Hiller A, Oikkonen M. QT interval, heart rate and
arterial pressures using propofol, thiopentone or methohexitone
for induction of anaesthesia in children. Acta Anaesthesiol
Sugammadex Efficacy During Anesthesia
ANESTHESIA & ANALGESIA