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PETSAVERS PAPER

An evaluation of a target-controlled
infusion of propofol or propofol
alfentanil admixture for sedation in
dogs
F. Montefiori*,1, P. Pawson*, A. Auckburally*, M. Scott and D. Flaherty*
*Division of Small Animal Clinical Sciences, Institute of Comparative Medicine, School of Veterinary Medicine, University of
Glasgow, Bearsden, Glasgow G12 8QQ

School of Mathematics and Statistics, University of Glasgow, Bearsden, Glasgow G12 8QW

Corresponding author email: Filippo.Montefiori@ed.ac.uk

OBJECTIVES: To evaluate sedation quality and cardiorespiratory variables in dogs sedated using a targetcontrolled infusion of propofol or propofolalfentanil admixture.
METHODS: A total of 60 dogs undergoing diagnostic imaging were randomly assigned to one of three
sedation protocols: propofol alone; propofol with a low concentration of 12 g of alfentanil per mL
of propofol; or propofol with a higher concentration of 24 g of alfentanil per mL of propofol. Targetcontrolled infusion was initiated at a propofol target concentration of 15 g/mL and increased until
lateral recumbency was achieved. Times to adopt lateral recumbency and recover, pulse rate, respiratory
rate, oscillometric mean arterial pressure and oxygen saturation were recorded. Quality of sedation
onset and recovery were scored.
RESULTS: Propofol target at lateral recumbency differed significantly (P=001) between groups with
median (range) values of 30 (15 to 55), 20 (2 to 45) and 225 (15 to 35) g/mL for propofol
alone, propofol with the lower concentration of alfentanil and propofol with the higher concentration of
alfentanil groups, respectively. Time to lateral recumbency was longer and quality of onset less smooth
for the propofol group. Pulse rate change differed significantly (P<0001) between groups (mean pulse
rate change at onset of sedation: propofol group +2 24 bpm, low concentration alfentanil group 30
24 bpm, higher concentration alfentanil group 26 23 bpm). Hypoxaemia (SpO2<90%) occurred in 1, 3
and 13 dogs, in the propofol group, the low concentration alfentanil group and the higher concentration
of alfentanil group, respectively (P<0001).
CLINICAL SIGNIFICANCE: Addition of alfentanil to propofol target-controlled infusion did not confer cardiovascular
benefits and, at the higher concentration, alfentanil increased the incidence of hypoxaemia.
Journal of Small Animal Practice (2016) 57, 181187
DOI: 10.1111/jsap.12459
Accepted: 28 January 2016

F. Montefioris current address is Department of Veterinary Anaesthesia, Royal (Dick) School of Veterinary Studies, Easter Bush Campus Midlothian EH25 9RG,
Edinburgh

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F. Montefiori et al.

INTRODUCTION
Sedation is commonly performed in veterinary medicine to
facilitate a range of procedures. A variety of sedative drugs are
available for use in the dog but most present disadvantages and,
to date, there is no single drug or combination which can guarantee reliable sedation coupled with fast onset and recovery plus
cardiorespiratory stability.
In animals, propofol use is generally limited to induction
(Morgan & Legge 1989) and maintenance of anaesthesia (Thurmon et al. 1994), and only occasionally administered for sedation
(Glowasky & Wetmore 1999). This contrasts with human medicine, in which propofol is commonly used to provide sedation for
a variety of procedures (Beller et al. 1988, Harper et al. 1991).
Propofol possesses several desirable characteristics for a sedative drug: it can provide a fast onset of sedation and rapid recovery (Crawford 1993), and has high total body clearance with
minimal accumulation following repeated doses or infusions
(Shafer et al. 1988). However, it causes dose-dependent cardiorespiratory depression (Mackenzie & Grant 1987, Dubois et al.
1988, Kuusela et al. 2003), and, given the high infusion rates that
are often necessary to prevent the patient responding, propofol
can cause hypotension and hypoventilation (Mackenzie & Grant
1985, Dubois et al. 1988). In addition, other adverse events
such as twitching, involuntary movement and muscle tremor
may occur (Hall & Chambers 1987, Sanderson & Blades 1988,
Davies 1991).
Although propofol is generally considered non-cumulative
when administered by constant-rate infusion, the plasma concentration of the drug does increase with time (Nolan & Reid
1993), potentially leading to worsening of cardiorespiratory
side-effects. In an attempt to avoid this accumulation, propofol
is now commonly administered as a target-controlled infusion
(TCI) in humans (Leslie et al. 2008), and its use in this way
has also been reported in dogs (Beths et al. 2001, Musk et al.
2005). With TCI, a microprocessor within an infusion pump is
programmed with the pharmacokinetic parameters for propofol
appropriate for the particular species, and an infusion control
algorithm based on a 1% propofol concentration. The anaesthetist inputs patient weight, age, and the desired plasma propofol concentration (target concentration). The processor, using
the algorithm, then calculates the rate of infusion required to
achieve and maintain the target propofol concentration (Leslie et
al. 2008); an initial bolus of the drug is delivered by the device
to rapidly attain the desired target, and a gradually decreasing
infusion is then delivered to maintain this concentration, thus
accounting for any potential accumulation of the drug over time.
The anaesthetist can change the target concentration depending
on the patient response; an increase in the selected target will lead
to the TCI device delivering a bolus of propofol to rapidly reach
the new target, followed by a higher infusion rate to maintain
this new target. Similarly, a decrease in the selected target will
lead to the system temporarily stopping the infusion until it calculates that the plasma concentration has decreased to the lower
target, followed by a slower infusion to then maintain that target.
A propofol TCI system, therefore, allows controlled titration
182

of plasma drug concentration with a consequent improvement

in haemodynamic and respiratory stability compared to manually controlled infusions (Passot et al. 2002, Breslin et al. 2004,
Leslie et al. 2008). For these reasons, propofol TCI to provide
sedation and anaesthesia has become commonplace in humans
(Lin et al. 2013). Relatively few reports describe propofol TCI in
dogs, although studies to identify appropriate target concentrations for induction and maintenance of anaesthesia considered
the technique to be safe and effective (Beths et al. 2001, Musk
et al. 2005). To date, there are no reports of the use of TCI for
sedation in dogs.
Attempts to minimise many of the undesirable effects of
propofol have led to its co-administration with opioid drugs in
humans (Hsieh et al. 2009). For sedation, propofol is commonly
used with alfentanil, a potent opioid with a similar pharmacokinetic profile to propofol, exhibiting rapid onset and minimal
accumulation in humans (Cookson 1983), with similar characteristics observed in dogs (Ilkiw et al. 1991). Human studies have
demonstrated a synergistic interaction between the two drugs,
leading to enhanced sedation and analgesia when compared to
propofol alone (Short et al. 1992, Pavlin et al. 1996). This reduces
the amount of propofol required to achieve sedation and may,
thereby, decrease associated side effects. In addition to simultaneous administration via separate infusions, a propofolalfentanil
mixture is chemically and pharmacodynamically stable, i.e. the
clinical effect of the two drugs remains the same if co-administered in the same syringe (Taylor et al. 1992, Engelhard et al.
1999).This so-called admixture is commonly used in humans
for sedation (Ho et al. 2012), although it is not free of complications and may cause respiratory depression (Yoon et al. 2011).
Propofolalfentanil combination, administered via TCI, can
be used to induce anaesthesia in dogs (Auckburally et al. 2008)
but there are no studies reporting its use for sedation in this species.
The aims of this study were to assess the quality of sedation
achieved using a TCI of propofol, either alone or in combination with one of two concentrations of alfentanil, to quantify
the propofol targets required in each group, and to evaluate the
cardiorespiratory effects of the sedation protocols.

MATERIALS AND METHODS

Animals
Approval to perform the study was obtained from the Ethics
Committee of the School of Veterinary Medicine, and the use of
alfentanil was authorised by the Veterinary Medicines Directorate (ATC-S-032).
A power calculation performed on pilot data showed that
inclusion of 18 dogs per group would detect a 05 g/mL difference in propofol target concentration between the groups with a
power of 80%.
Sixty client-owned dogs of American Society of Anesthesiologist physical status I or II, undergoing diagnostic imaging for
orthopaedic conditions, were included. Dogs were of various
breeds, aged between eight months and eight years and weighing

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between 8 and 50 kg. Subjects were excluded if they were brachycephalic, markedly underweight or obese, or if they were receiving
concurrent drug therapy that could influence the sedation, such
as opioids or anticonvulsants.
Study design/study protocol
Dogs were randomly allocated to 3 treatment groups (n=20) using
computer-generated random numbers: group P received propofol alone (Vetofol, Norbrook Laboratories Limited); group PA12
received a propofol-alfentanil admixture, prepared by diluting
1.2 mL of 600 g alfentanil (Rapifen, Jansenn-Cilag Ltd) with
1% propofol to a total volume of 50 mL, resulting in a final concentration of 12 g/mL alfentanil in the admixture; group PA24
received a propofol -alfentanil admixture prepared by diluting
2.4 mL of 1200 g alfentanil with 1% propofol to a total volume
of 50 mL, giving a final concentration of 24 g/mL alfentanil.
The anaesthetist sedating the animals (FM) was unaware of the
treatment group because the syringes were prepared by other
anaesthetists.
Before sedation, a cannula was placed in a peripheral vein and
baseline cardiorespiratory variables, including heart rate, pulse
rate, respiratory rate and non-invasive arterial blood pressure
(Cardell veterinary monitor, Model 9401, Sharn Veterinary Inc.),
were recorded.
Each dogs age and body weight were programmed into the
TCI device (Diprifusor, AstraZeneca) and sedation initiated using
a plasma propofol target of 15 g/mL. Three minutes later (to
allow sufficient time for the drugs to reach an appropriate effect
site concentration), each dog was assessed and if it had not adopted
lateral recumbency, the propofol target was further increased by
an increment of 05 g/mL. These increments were repeated every
3 minutes until lateral recumbency was achieved, and the target
plasma concentration was thereafter altered as appropriate, based
on the animals response to the procedure being undertaken.
Monitoring and data collection
Time to achieve lateral recumbency was recorded. The quality of
the onset of sedation was assessed and scored by the same blinded
observer (FM) considering the occurrence, degree and duration
of adverse events such as paddling, muscle rigidity or vocalisation
(Table A1).
Throughout the period of sedation, pulse rate, respiratory
rate, SpO2 (Model 9847 V, Nonin, Medical Inc.) and oscillometrically derived arterial blood pressure (Cardell veterinary monitor, Model 9401, Sharn Veterinary Inc.) were recorded every 2
minutes unless incompatible with the diagnostic procedure. A
Mindray Mec-1200 multiparameter monitor (Mindray, Medical
International Limited) was used to monitor the ECG. Any episodes of bradycardia (pulse rate <60 per minute) or hypotension
(MAP <60 mmHg) were recorded.
Reflexes were frequently assessed to judge depth of sedation
and ensure that dogs were able to control their airway; the presence of tongue withdrawal and a brisk palpebral reflex were taken
to indicate that a patient was sedated rather than anaesthetised.
The target propofol concentration was adjusted as required, to
facilitate the diagnostic procedure while avoiding loss of airway
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control, and all changes in the target concentration were recorded.

Being clinical cases, the sedated dogs were subject to varying
degrees of stimulation, such as joint manipulation or variations
in positioning. All other events that could have impacted on the
sedation status (e.g. excessive room noise) were also recorded.
Adverse events, such as hypoxaemia (SpO2<90%), paddling
and/or muscle rigidity, were noted. Oxygen was administered,
using a face mask, to any dog demonstrating hypoxaemia.
If marked paddling and/or muscle rigidity developed,
these were treated by increasing propofol target concentration; if this proved unsuccessful or the intensity of paddling/
muscle rigidity was incompatible with the diagnostic procedure, sedation was converted to general anaesthesia with
endotracheal intubation, and maintenance using isoflurane.
At the end of the procedure, the infusion was stopped and the
patient was allowed to recover in a quiet room. Time for recovery
was recorded, and the quality of recovery was evaluated considering the presence and degree of adverse events such as paddling,
vocalising and ataxia. The patients were then allocated to different
groups following the scoring system in Table A2.
Throughout the study, all data collection and scoring was performed by the same blinded observer (FM).
Statistical analysis
Data were analysed using Microsoft Excel and Minitab (Minitab
Release 16). All variables were tested for normality. Weight and
cardiovascular variables (normally distributed data) were analysed
using one-way analysis of variance with post-hoc Tukey test. Age,
propofol target to achieve lateral recumbency, and times to adopt
lateral recumbency with the onset of sedation, and to recover to
sternal and standing positions, were analysed using KruskalWallis test with post-hoc MannWhitney test. Gender, quality of
onset of sedation and recovery and all adverse events (categorical
data) were analysed with Pearsons chi-squared test with post-hoc
two-proportion test. To facilitate analysis of scores for onset of
sedation and for recovery, dogs scoring 1 and 2 were compared to
dogs scoring 3 and 4. A correlation test was performed to assess
the linear relationship between the time required to assume sternal and standing positions and the duration of sedation.
When comparing the three groups, differences were considered significant with P<005. During post-hoc testing the
P value was adjusted for multiple comparisons.

RESULTS
Animals
Twenty dogs were allocated to each group. Of these 38 were male
and 22 female. The dogs weighed 256 113 kg (meansd) and
were 597 258 months old (meansd). There were no significant differences between groups with respect to sex (P=0256),
weight (P=0309; mean: group P 226 98 kg, group PA12 263
112 kg, group PA24 279 127 kg) or age (P=0445; median:
group P 685 months, range 21 to 96, group PA12 565 months,
range 11 to 94, group PA24 546 months, range 10 to 96). One
patient from group PA24 developed sustained muscle rigidity

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F. Montefiori et al.

and had to be anaesthetised to facilitate diagnostic imaging and

was excluded from the study.
Propofol target, sedation and recovery
characteristics
The propofol target concentrations required to achieve lateral
recumbency are shown in Figure 1. Median (range) values for
groups P, PA12 and PA24 were 3 (15 to 55), 2 (2 to 45) and
225 (15 to 35) g/mL, respectively. A significant difference was
found between the groups (P=0010) and post-hoc comparisons
revealed that group P required a higher target concentration than
groups PA12 (P=0013) and PA24 (P=0011).
Time to achieve lateral recumbency differed significantly
between groups (P=0019; Table 1). Patients in group P took
longer to achieve lateral recumbency compared to groups PA12
(P=0013) and PA24 (P=0012), median (range) values being
105 (3 to 27), 6 (6 to 21) and 75 (3 to 75) minutes, respectively.
Statistical differences between groups were found when assessing the quality of onset of sedation [group P 2 (1 to 4), group
PA12 1 (1 to 4), group PA24 1 (1 to 3), P=0040] (Table 1).
Patients in the PA24 group had a significantly smoother onset
of sedation when compared with patients in group P (P=0001).
No significant differences were found between the groups when
considering time to achieve sternal (median values: group P 12
minutes, range 2 to 30, group PA12 9 minutes, range 3 to 26,
and group PA24 6 minutes, range 1 to 18, P=0134) and standing positions (median values : group P 20 minutes, range 5 to 39,

FIG 1. Plasma target concentrations of propofol (median, IQR and range)

required to produce lateral recumbency in dogs sedated with propofol
alone (P, n=20), propofol with 12 g/mL alfentanil (PA12, n=20) or
propofol with 24 g/mL alfentanil (PA24, n=19). Propofol target for P
is significantly higher than for PA12 (P=0013) and PA24 (P=0011).
Median values for group PA12: 2 (2 to 45). t = outliers

group PA12 17 minutes, range 8 to 40, group PA24 12 minutes,

range 6 to 44, P=0064), or the quality of recovery [group P 1 (1
to 3), group PA12 1 (1 to 3), group PA24 1 (1 to 4), P=0459]
(Table 1).
Duration of sedation was not different between groups
(P=0853): median (range) values for groups P, PA12 and PA24
were 475 (27 to 108), 475 (31 to 78) and 45 (28 to 96) minutes, respectively. However, statistically significant weak-to-moderate positive correlations were found between the duration of
sedation and the time to achieve sternal (r=0323, P=0013) and
standing positions (r=0511, P=0001).
Cardiovascular variables
Pulse rates and mean arterial pressure (MAP) are shown in Table
2. No difference in baseline pre-sedation pulse rate (PR0) was
found between groups (mean PR0: group P 97 20 bpm, group
PA12 112 20 bpm, group PA24 107 17, P=0053). The first
pulse rate recorded once lateral recumbency was achieved (PR1),
differed significantly between groups and was lower in groups
PA12 and PA24 when compared to group P (mean PR1: group P
99 21 bpm, group PA12 83 19 bpm, group PA24 81 18 bpm,
P=0007). The change in PR with the onset of sedation (PR1
PR0) followed a similar pattern, PR falling in groups PA12 and
PA24 but not group P (mean PR1PR0 : group P +2 24 bpm,
group PA12 30 24 bpm, group PA24 26 23 bpm, P<0001).
Baseline MAP, measured before sedation, did not differ significantly between groups (mean MAP: group P 126
21 mmHg, group PA12 117 23 mmHg, group PA24 124
20 mmHg, P=0376). Once lateral recumbency was achieved,
the first recorded blood pressure, MAP1, was lower in group
PA12 compared to the other groups (mean MAP1: group P 100
213 mmHg, group PA12 86 122 mmHg, group PA24 102
20 mmHg, P=0004). However, when the change in MAP
(MAP1MAP0) was considered, it was found to be similar in all
groups (mean MAP1MAP0: group P 25 29 mmHg, group
PA12 31 28 mmHg, group PA24 22 29 mmHg, P=0591).
Adverse events
Paddling occurred in five dogs (four in group P and one in group
PA12) and muscle rigidity occurred in 12 dogs (three in group
P, four in group PA12 and five in group PA24). No statistically
significant difference in occurrence was found between groups
for either event (paddling: P=0064, muscle rigidity: P=0680).
Although of variable duration, all these adverse events resolved
during the procedure itself or early in the recovery period, with
the exception of one animal in group PA24, in which sustained

Table 1. Speed and quality of sedation and recovery

Onset of sedation
Recovery from sedation

Time to lateral recumbency (minutes)

Score for quality of sedation
Time to sternal recumbency (minutes)
Time to standing position (minutes)
Score for quality of recovery

PA12

PA24

P Value

105 (3 to 27)
2 (1 to 4)
12 (2 to 30)
20 (5 to 39)
1 (1 to 3)

6 (6 to 21)
1 (1 to 4)
9 (3 to 26)
17 (8 to 40)
1 (1 to 3)

75 ( 3 to 75)
1 (1 to 3)
6 (1 to 18)
12 (6 to 44)
1 (1 to 4)

0019
0040
0134
0064
0459

The speed and quality of sedation onset and recovery in dogs sedated with propofol alone (P) or combined with two different concentrations of alfentanil (PA12 and PA24). Results are
expressed as median (range)

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Table 2. Cardiovascular variables

Base-line PR0
First sedated PR1
PR change (PR1PR0)
Base-line MAP0
First sedated MAP1
MAP change (MAP1MAP0)

Group P

Group PA12

Group PA24

P Value

9720
9921
224
12621
100213b
2529

11220
8319a
3024a
11723
86122
3128

10717
8118a
2623a
12420
10220b
2229

0053
0007
<0001
0376
0004
0591

Pulse rates (PR) and mean arterial blood pressures (MAP) recorded in dogs sedated with propofol alone (P) or in combination with two different concentrations of alfentanil (PA12 and PA24).
Data are reported as mean sd
a significantly different from group P
b significantly different from group PA12

muscle rigidity was incompatible with the procedure, and the

dog was therefore anaesthetised and excluded from the study.
Paddling of the forelimbs and muscle rigidity of both fore- and
hind limbs were observed in this patient 3 minutes after achieving lateral recumbency, at a propofol target of 3 g/mL. Paddling
disappeared when the propofol target was increased to 6 g/mL
but muscle rigidity remained. The propofol target was further
increased to 7 g/mL, at which point the SpO2 decreased below
90%; this was successfully managed by administering oxygen via
face mask. Because muscle rigidity persisted, the propofol target
was increased to 8 g/mL and, despite oxygen administration,
the SpO2 again fell below 90%. The decision was then taken to
induce general anaesthesia with a propofol bolus, intubate the
trachea and maintain anaesthesia with isoflurane in oxygen.
SpO2 immediately returned to normal, and muscle rigidity disappeared within approximately 2 minutes. Bradycardia occurred
in four dogs in group PA12 (lowest PR 48 bpm) and five in group
PA24 (lowest PR 49 bpm). One dog in group P (lowest MAP
58 mmHg ) and two in group PA24 (lowest MAP 53 mmHg )
became hypotensive. In all cases bradycardia and hypotension
were transient and no treatment was administered.
Seventeen dogs became hypoxaemic, with a significantly
greater incidence (P<0001) in group PA24 (13/19), when compared to groups P (1/20) and PA12 (3/20). Hypoxaemia was
successfully resolved by providing supplemental oxygen via face
mask.

DISCUSSION
In this study, combining alfentanil with propofol decreased
the propofol target concentration required to produce lateral
recumbency in dogs requiring sedation for diagnostic imaging
compared with propofol alone. These findings are similar to the
results in human patients, in which the addition of an opioid also
reduced the required dose of propofol for sedation (Pavlin et al.
1996). In the veterinary literature, use of a propofol-alfentanil
admixture to achieve sedation has not previously been reported.
However, use of the combination to induce general anaesthesia has been evaluated in dogs: in this context, and using a TCI
device, alfentanil was also demonstrated to have a propofol-sparing effect (Auckburally et al. 2008).
Although our data show that addition of alfentanil decreases the
propofol target required, increasing the alfentanil concentration
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from 12 to 24 g/mL did not lead to a further reduction in propofol target, suggesting a possible ceiling effect. This is similar
to the findings of Auckburally et al. (2008), who reported that a
higher alfentanil dose did not further decrease hypnotic requirements for induction of anaesthesia.
Addition of alfentanil to propofol hastened the onset of sedation in both PA12 and PA24 when compared to group P, although
this was potentially because of the lower targets required in the
former two groups and the slow upward titration method used
in this study. In addition, the quality of the onset of sedation was
positively influenced by inclusion of the high concentration of
alfentanil in the protocol. However, the frequent occurrence of
paddling and/or muscle rigidity affected the quality of sedation
in many cases during the maintenance phase of the procedure,
although there were no differences in the incidence of these events
between groups. Neither was there a difference in the quality of
recovery between groups. In both human and veterinary medicine, propofol reactions, such as twitching, involuntary movement and muscle tremor have been previously reported (Hall &
Chambers 1987, Sanderson & Blades 1988, Davies 1991) with
variable incidence (75 to 217%). In our study, 233% of dogs
developed at least one of these adverse events, possibly because
our dogs were only sedated (and, therefore, likely had lower
plasma propofol concentrations) compared to studies in which
patients were anaesthetised. In addition, alfentanil-related muscle rigidity has been described as a side-effect in humans (Benthuysen et al. 1986).
Even at sedative doses, propofol can induce cardiovascular depression (Wehrmann et al. 1999). Given that alfentanil is
relatively cardiostable (DAubioul et al. 1984), the reduction
in propofol target produced by alfentanil might, therefore, be
expected to improve the haemodynamic profile. In this study,
with the onset of sedation, mean pulse rate remained relatively
stable in the propofol group but fell in the groups receiving the
propofolalfentanil combinations. Although unlikely to be of
any real clinical significance, the first MAP measurement at the
onset of sedation was significantly lower in PA12 compared to
both other groups. The reason for this finding, especially the difference between PA12 and PA24 is unclear. Baseline MAP was
lower in group PA12, and although this difference was not statistically significant, it may have contributed to the lower MAP at
the onset of sedation. When the change in MAP with the onset
of sedation was examined it was found to be of similar magnitude in all groups. These findings are consistent with those of

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F. Montefiori et al.

Auckburally et al. (2008) who also demonstrated that, despite a

reduction in propofol target required for induction of anaesthesia, propofolalfentanil admixture did not lessen the reduction
in arterial pressure, when compared to propofol alone. Although
a number of dogs in the study were classed as bradycardic and/
or hypotensive, these effects were transient and treatment was
not required. In summary, we could demonstrate no beneficial
cardiovascular effects from either propofol-alfentanil admixture
compared to propofol alone.
Group PA24 demonstrated a relatively high incidence of
hypoxaemia, which is in agreement with human studies reporting an increased risk of hypoxaemic events during sedation with
propofol-alfentanil, compared to propofol alone, and a synergistic interaction with respect to respiratory depression has been
proposed (Pavlin et al. 1996, Yoon et al. 2011). The marked
difference in the incidence of hypoxaemia between PA12 and
PA24, in this study, would suggest that alfentanil is exerting a
dose-dependent effect in this regard. Although drug-related
hypoventilation is the likeliest cause of the hypoxaemia observed
in this study, measurement of end-tidal carbon dioxide (EtCO2)
or partial pressure of carbon dioxide in the arterial blood would
be required to confirm this. Given that this was a clinical study,
arterial sampling could not be justified. Measurement of EtCO2
was attempted via nasal prongs, but this was abandoned because
most dogs would not tolerate their placement despite being
sedated.
A propofol TCI system was used to administer propofol and
the propofolalfentanil admixtures in this study. This system uses
a pharmacokinetic model which assumes a 1% propofol concentration. When adding another drug, such as alfentanil in this
study, propofol concentration decreases and the system precision
therefore may be affected. In the present study, the addition of
12 mL (PA12) and 24 mL (PA24) of alfentanil in the two admixtures caused a reduction in the propofol concentration from 1 to
0976% (PA12) and 0952% (PA24), respectively. These minimal changes in concentration are unlikely to be clinically relevant
as the admixtures were titrated to effect, and because there are
always pharmacokinetic differences within any population.
The animals included in this study were drawn from a clinical and, therefore, variable population, in terms of patient temperament and the degree of stimulation during the diagnostic
imaging. Although the majority of dogs presented with similar
orthopaedic conditions and underwent comparable diagnostic
imaging procedures, the degree of pre-existing pain or discomfort could not be standardised and may have led to differing levels of stimulation during positioning. One potential advantage
of a TCI system for provision of sedation in this regard is that,
unlike conventional sedative techniques, the infusion can be
specifically titrated in line with the patient response to stimulation, thus potentially minimising periods of over- or undersedation. Avoiding excessive sedation is important because this
should minimise the risk of the animal progressing towards general anaesthesia, and potentially then losing control of its airway.
During this study, patient reflexes were assessed frequently and
the plasma target was reduced in response to signs of excessive
sedation.
186

In conclusion, this study demonstrated that addition of alfentanil to a propofol TCI technique significantly reduced the propofol target concentration necessary to achieve lateral recumbency
in dogs requiring sedation. However, this propofol-sparing effect
did not provide any cardiorespiratory benefits, and the higher
concentration of alfentanil significantly increased the incidence
of hypoxaemia. Finally, although effective for many dogs in this
study, the protocol was not considered suitable for all patients
because of the frequent occurrence of muscle rigidity and
paddling.
Acknowledgements
This study was made possible through financial support from
Pertsavers (ref. CTP 23.11), who also funded Filippo Montefioris veterinary anaesthesia residency training programme (ref.
CTP 20.11).
Conflict of interest
None of the authors of this article has a financial or personal
relationship with other people or organisations that could inappropriately influence or bias the content of the paper.
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APPENDIX
Table A1. Scoring system used to categorise onset of
sedation
Score

Quality of onset of sedation

Smooth transition (i.e. no paddling), no twitching or muscle

rigidity
Occasional slow paddling movements or occasional mild
muscle twitching or muscle rigidity
Moderate sustained paddling movements, sustained muscle
twitching or muscle rigidity
Marked paddling, struggling or vocalisation and/or severe
twitching with opisthotonus and/or extensor rigidity

2
3
4

Table A2. Scoring system used to categorise quality of

recovery
Score

Quality of recovery

1
2
3
4

Good: quiet, no paddling or vocalising, no or minimal ataxia

Fair: some paddling or vocalising or moderate ataxia,
Poor: paddling and vocalising or marked ataxia
Very Poor: vocalising and thrashing, at risk of injury if not
restrained

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