Veterinary Anaesthesia and Analgesia, 2009, 36, 18–24
RESEARCH PAPER
Effects of changing body position on oxygenation and
arterial blood pressures in foals anesthetized with
guaifenesin, ketamine, and xylazine
Christina Braun Dr Med.Vet., Cynthia M Trim
Randy B Eggleston DVM, Diplomate ACVS
Department of Large Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
Correspondence: Christina Braun, Department of Large Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia,
Athens, GA 30602-5023, USA. E-mail: cbraun@uga.edu
Abstract
Objective To investigate the impact of a change in
body position on blood gases and arterial blood
pressures in foals anesthetized with guaifenesin,
ketamine, and xylazine.
Study design Prospective, randomized experimental
study.
Animals Twelve Quarter Horse foals, age of 5.4 ±
0.9 months and weighing 222 ± 48 kg.
Methods Foals were anesthetized with guaifenesin,
ketamine, and xylazine for 40 minutes in lateral
recumbency and then assigned to a change in lateral
recumbency after hoisting (Group 1, n = 6), or no
change (Group 2, n = 6). Oxygen 15 L minute)1
was insufflated into the endotracheal tube through-
out anesthesia. Arterial blood pressure, heart rate,
respiratory rate (fR), inspired fraction of oxygen
(FIO2), and end-tidal carbon dioxide (PE¢CO2) were
measured every 5 minutes. Arterial pH and blood
gases [arterial partial pressure of oxygen (PaO2),
arterial partial pressure of carbon dioxide (PaCO2)]
were measured at 10, 30, and 40 minutes after
induction, and 5 minutes after hoisting. Alveolar
dead space ventilation and PaO2/FIO2 were calcu-
lated. Two repeated measures models were used. All
hypothesis tests were two-sided and significance
level was a = 0.05. All values are presented as least
square means ± SE.
18
doi:10.1111/j.1467-2995.2008.00423.
BVSc, DVA, Diplomate ACVA, Diplomate ECVAA, MRCVS &
Results Values at time-matched points from the two
groups were not significantly different so they were
combined. Arterial partial pressure of oxygen
decreased significantly from 149 ± 14.4 mmHg
before hoisting to 92 ± 11.6 mmHg after hoisting
(p = 0.0013). The PaO2/FIO2 ratio decreased from
275 ± 30 to 175 ± 24 (p = 0.0055). End-tidal car-
bon dioxide decreased significantly from 48.7 ± 1.6
to 44.5 ± 1.2 mmHg (p = 0.021). Arterial partial
pressure of carbon dioxide, blood pressures and
heart rates measured 5 minutes after hoisting were
not different from measurements obtained before
hoisting.
Conclusion and clinical relevance Hoisting
decreased PaO2 in anesthetized healthy foals.
Administration of supplemental oxygen is recom-
mended to counter the decrease in oxygenation and
PaO2 measurement is necessary to detect early
changes.
Keywords anesthesia, body position, horses, keta-
mine, oxygenation.
Introduction
Induction of anesthesia with injectable or inhalant
agents is associated with significant changes in
arterial oxygen tension (PaO2) when compared with
values in conscious or sedated horses (Hall et al.
1968; Ellis et al. 1977; Muir et al. 1978; Schatz-
mann et al. 1982; Hubbell et al. 1989; Wan et al.
 Hoisting decreased PaO2 in anesthetized horses C Braun et al.
1992; Muir & Mason 1993; Cuvelliez et al. 1995).
This decrease in PaO2 is attributed to increased
ventilation–perfusion mismatch (V/ _ Q_ mismatch)
and intra-pulmonary shunts that develop as a result
of recumbency-induced decreases in lung volume
and redistribution of perfusion (McDonell et al.
1979; Sorenson & Robinson 1980; Stegmann &
Littlejohn 1987; Nyman & Hedenstierna 1989;
Nyman et al. 1990; Marntell et al. 2005a,b).
Abrupt decreases in PaO2 have been measured in
anesthetized horses with a change in recumbency
(Hall 1979; McDonell et al. 1979; Gleed & Dobson
1988; Gasthuys et al. 1991) and when horses were
rolled into different lateral recumbencies during
recovery from anesthesia (Mason et al. 1987). We
proposed to investigate the impact of body change
on some cardiopulmonary parameters in foals
anesthetized with guaifenesin, ketamine, and
xylazine.
Materials and methods
This research project was approved by the local
Institutional Animal Care and Use Committee.
Twelve Quarter Horse foals, eight males and four
females, aged of 5.4 ± 0.9 months (mean ± SD)
(range 4–7 months) and weighing 222 ± 48 kg
(range 109–268 kg), were anesthetized for splint
bone biopsies as part of a different research project
involving a feeding trial. All foals were considered
healthy on the basis of history and clinical exami-
nation findings. Six male foals were assigned to a
change in recumbency after hoisting (Group 1).
Four female and two male animals did not undergo
a change in recumbency after hoisting (Group 2).
The mean ages of the foals in Groups 1 and 2 were
the same at 5.4 ± 0.4 months, and the mean body
weights were 218 ± 16 kg and 227 ± 24 kg,
respectively.
Food was withheld for 12 hours prior to anes-
thesia with free access to water. The foals were
sedated with xylazine (0.4 mg kg)1, Sedazine,
100 mg mL)1; Fort Dodge Animal Health, Fort
Dodge, IA, USA) intravenously (IV), a minimum of
30 minutes before anesthesia. After subcutaneous
infiltration of 1 mL of 2% lidocaine (Abbott Labo-
ratories, North Chicago, IL, USA) a 14-SWG cath-
eter (Jorvet; Jorgensen Laboratories, Inc., Loveland,
CO, USA) was inserted into a jugular vein. The foals
received phenylbutazone (4.4 mg kg)1 intravenous
(IV), Butaject; Butler, St Joseph, MO, USA) and
potassium penicillin G (22 000 IU kg)1 intramus-
 2009 University of Georgia, 36, 18–24
cular (IM); G.C. Hanford Mfg. Co., Syracuse, NY,
USA).
The foals were pre-medicated with xylazine
(1.1 mg kg)1) and butorphanol (0.02 mg kg)1,
Torbugesic, 10 mg mL)1; Fort Dodge Animal
Health), IV. Anesthesia was induced 3 minutes
later with ketamine (2.2 mg kg)1, Ketaset HCl,
100 mg mL)1; Fort Dodge Animal Health) IV and
maintained for 50 minutes by IV infusion (Volu-
metric pump Flo-Gard 620; Baxter Diagnostics,
Deerfield, IL, USA) of a combination of guaifenesin,
ketamine, and xylazine (GKX, 1300 mg ketamine
and 650 mg xylazine in 1 L 5% guaifenesin,
Guaifenesin injection; Phoenix Scientific Inc.,
St Joseph, MO, USA). The GKX mixture was
prepared just before anesthesia and the infusion of
2 mL kg)1 hour)1 was started as soon as the foals
were recumbent after induction of anesthesia. Three
volumetric pumps were used in this study and the
calibration of each was verified by timed collection
of fluid into a graduated cylinder.
After induction of anesthesia, the tracheas were
intubated with a 22-mm ID cuffed Murphy endo-
tracheal tube (Bivona; Smith Medical International
Ltd., Kent, UK), except for the smallest one that
was intubated with a 20-mm ID tube. Oxygen,
15 L minute)1, was insufflated through tubing
extended 15 cm into the endotracheal tube. The
flowmeter calibration was checked using a Wright’s
respirometer (Ainca Inc., Hudson, NY, USA) before
anesthesia by recording gas flow over 1 minute.
A gas sampling tube had been pre-placed within the
lumen of the endotracheal tube with the tip close to
the Murphy eye end of the tube. The distance
between the oxygen insufflation tube and the gas
sampling tube was 75 cm. During anesthesia, the
sampling tube was connected to a gas analyzer
(Poet IQ; Criticare Systems Inc., Waukesha, WI,
USA) for measurement of inspiratory oxygen con-
centration (FIO2), end-tidal carbon dioxide concen-
tration (PE¢CO2), and fR. The gas analyzer was
calibrated each experimental day with gases con-
taining 5% carbon dioxide and zero oxygen
obtained from the manufacturer.
A 20- or 22-SWG, 2.5 cm catheter (SureFlo;
Terumo Medical Corporation, Elkton, MD, USA) was
inserted into a facial or transverse facial artery and
connected to a pressure transducer (TruWave Dis-
posable Pressure Transducer; Edwards Lifesciences
LLC, Irvine, CA, USA) and a multiparameter physi-
ologic monitor (Ultraview 90367; Spacelabs Health-
care, Issaquah, WA, USA). The transducer was
19
Hoisting decreased PaO2 in anesthetized horses C Braun et al.
placed at the level of the thoracic inlet to facilitate
measurement of arterial blood pressures, and heart
rates. The transducers were zeroed electronically.
The duration of the surgical procedure varied among
animals; the average time for start and finish was
9 and 23 minutes after induction of anesthesia,
respectively.
Experimental design
The initial recumbent position, and the option for
change in body position, were assigned at the start
of the study by random selection using a latin
square design. Induction of anesthesia was accom-
plished by a free fall on to a 25-cm-thick foam mat
with the foal in pre-assigned left or right lateral
recumbency. After 40 minutes of anesthesia, the
foals were hoisted for 1 minute by means of hobbles
applied to all four legs distal to the fetlocks and
attached to a central ring. They were then either
returned to the original position (n = 6) or lowered
into the opposite lateral recumbency (n = 6).
Anesthesia was continued for 5 minutes after
hoisting.
Arterial blood pressure (AP), heart rate, fR, FIO2,
and PE¢CO2 were measured at 5-minute intervals
after induction of anesthesia, and 5 minutes after
hoisting. Blood was aspirated from the arterial
catheter and discarded before arterial blood was
collected anerobically into heparinized 3 mL plastic
syringes for measurement of pH and blood gases
(PaO2, PaCO2) at 10, 30, and 40 minutes after
induction of anesthesia, and 5 minutes after hoist-
ing. Rectal temperature was measured at each
collection time. One blood sample was collected
before hoisting for measurement of hemoglobin
concentration. All blood samples were stored in ice
water until analyzed within 60 minutes (Stat Profile
Ultra; Nova Biomedical, Waltham, MA, USA). Blood
gas values were corrected to rectal temperature.
Nasal insufflation of oxygen, 15 L minute)1, was
provided after endotracheal extubation. The foals
recovered without assistance on the foam mat in the
same stall with a low level light intensity. The time
taken from the end of anesthesia until the foals were
standing was recorded. The quality of recovery was
scored as 1 = excellent, standing at first attempt;
2 = good, quiet recovery with two to three unsuc-
cessful attempts at standing; 3 = adequate, quiet
recovery with multiple attempts to stand; and
4 = rough, multiple vigorous or uncontrolled
attempts to stand.
20
Calculations
Estimate of alveolar dead space fraction (V_ D) was
calculated as
V_ D ¼ ðPaCO2  PE0 CO2 Þ=PaCO2
Ratio between PaO2 and FIO2 ¼ ðPaO2 =FIO2 Þ
Statistical analysis
Two multi-variant repeated measures models were
used. Both of them recognized multiple observations
as belonging to the same horse to test for differences
in measured clinical parameters between foals:
First, the impact of recumbency and its change on
cardiopulmonary variables were modeled using
solely the data immediately before (40 minutes)
and after (46 minutes) hoisting; accounting for the
following differences:
(a) Initial left recumbency and initial right
recumbency.
(b) No change in lateral recumbency and change
in lateral recumbency.
(c) Before hoisting and after hoisting.
In the second model, we evaluated the effect of
time on these variables before hoisting, i.e. from 10
to 40 minutes after induction of anesthesia.
Applicable interaction terms were all >0.05 and
were therefore removed from the model. The
Tukey–Kramer adjustment was used for paired
comparisons over time. An unstructured covariance
structure was used in all repeated measures models.
Recovery times and recovery scores between foals
undergoing a change in recumbency and foals with
no change in recumbency were compared using a
t-test. All hypothesis tests were two-sided and the
significance level was a = 0.05. The statistical
analysis was performed using PROC MIXED in
SAS V 9.1 (Cary, NC, USA). Results are presented
as least square means ± SE unless otherwise noted.
Results
The time between administration of xylazine for
jugular vein catheterization and beginning of
anesthesia ranged from 30 to 407 minutes
(158 ± 66 minutes) in Group 1 and 93–274
minutes (178 ± 27 minutes) for five foals in
Group 2. The time of xylazine administration for
jugular vein catheterization was not recorded in one
foal in Group 2.
 2009 University of Georgia, 36, 18–24
 Hoisting decreased PaO2 in anesthetized horses C Braun et al.
Retrospective calculation of the volumes adminis-
tered by the infusion pumps revealed a range
of anesthetic delivery from 1.76 to 1.92 mL
kg)1 hour)1 (up to 8.8% difference from the intended
delivery). The average volume of anesthetic solution
administered to the two groups was equal
(1.82 mL kg)1 hour)1 for Group 1 and 1.88 mL
kg)1 hour)1 for Group 2). A GKX infusion rate of
1.82 mL kg)1 hour)1 corresponds to guaifenesin
91 mg kg)1 hour)1, ketamine 2.37 mg kg)1 hour)1,
and xylazine 1.18 mg kg)1 hour)1. One foal in
Group 2 turned its neck during the hoisting process
but none of the other animals moved.
No statistically significant differences in cardio-
pulmonary parameters were identified between foals
initially placed in either left or right lateral recum-
bency. There were no statistically significant differ-
ences in any measured parameter between foals
placed into the contralateral recumbency (Group 1)
after hoisting versus foals returned into the original
recumbency (Group 2). Therefore, measured values
from both groups were combined.
One foal was found to be disconnected from
oxygen for the first 15 minutes of anesthesia and
this animal’s corresponding arterial blood gas
results were subsequently removed from the statis-
tics. Insufflation of the endotracheal tubes with
oxygen resulted in an average FIO2 of 0.54 ± 0.08.
In our first statistical model comparing measure-
ments obtained immediately before and after hoisting
respiratory data were significantly different (Fig. 1).
Arterial oxygenation (PaO2) decreased significantly
from 149 ± 14.4 mmHg before hoisting to 92 ±
11.6 mmHg after hoisting (n = 12, p = 0.0013).
The PaO2/FIO2 ratio decreased from 275 ± 30 to
175 ± 24 (p = 0.0055). PE¢CO2 decreased signifi-
cantly from 48.7 ± 1.6 to 44.5 ± 1.2 mmHg
(p = 0.021). Arterial partial pressure of carbon
dioxide did not significantly change. Estimated dead
space ventilation increased from 5.4% to 13%.
However, this change was not statistically significant
(p = 0.066). Arterial blood pressures and heart rates
measured 5 minutes after hoisting were not different
from measurements obtained before hoisting.
Results from our second statistical model looking
at temporal changes on studied variables showed
significant decreases in AP, PE¢CO2, PaO2, and
temperature from 10 to 40 minutes after induction
of anesthesia. V_ D, pHa, HCO3), and Base Excess
increased over time (Table 1).
Group 1 foals were standing at 27 ± 6.7 minutes
(2–48 minutes) and Group 2 foals at 41 ± 5.3 min-
 2009 University of Georgia, 36, 18–24
Figure 1 Ventilatory changes before and after hoisting in
12 foals anesthetized with guaifenesin, ketamine and
xylazine, and receiving oxygen supplementation. All values
are presented as least square means ± SE (*p < 0.05).
utes (23–56 minutes), after discontinuation of GKX
infusion. Recovery times of the two groups were not
statistically different (p = 0.124). Recovery scores of
Groups 1 and 2 were 1.3 ± 0.2 and 1.7 ± 0.3,
respectively, and were not statistically different.
One foal in Group 1 was observed to have
excessive abdominal distension on recovery. The
nasal oxygen tube was removed and the foal stood
up at 24 minutes with a recovery score of 1
(excellent). No treatment was necessary.
Discussion
In this study, PaO2 decreased by an average of
20 mmHg from 10 to 20 minutes after induction of
anesthesia, and by 7 mmHg between 30 and
40 minutes of anesthesia indicating a progressive
decline. In contrast, hoisting the foals at 40 minutes
of anesthesia resulted in a decrease of 57 mmHg
measured 5 minutes later. As the change in PaO2
that occurred with hoisting was greater and more
abrupt than the temporal change, it is unlikely that
the decrease following hoisting can be attributed
only to time. Nevertheless, as a result of the use of
two statistical models, a direct comparison cannot
take place. The predictions of PaO2 based on the
different models at the last measurement before
hoisting (40 minutes) were statistically indistin-
guishable, i.e. within one confidence interval of each
other. A combined analysis could have been used to
compare the cardiopulmonary effects over all time
points including post-hoisting data if a greater
number of foals had been included in the study.
A decrease in PaO2 can be caused by a low frac-
tion of inspired oxygen, hypoventilation, diffusion
21
Hoisting decreased PaO2 in anesthetized horses C Braun et al.

Table 1 Temporal changes of cardiorespiratory parameters in 12 foals anesthetized with guaifenesin, ketamine and
xylazine, and receiving oxygen supplementation

Time (minutes) after induction of anesthesia Significance

p < 0.05
Parameter 10* 30 40 Between time-points

Arterial blood pressures (mmHg)

Systolic 142 ± 5 128 ± 5 123 ± 5 10–30, 10–40, 30–40
Diastolic 103 ± 4 89 ± 4 84 ± 4 10–30, 10–40, 30–40
Mean 118 ± 4 104 ± 4 99 ± 4 10–30, 10–40, 30–40
HR (beats minute)1) 40 ± 1 41 ± 1 41 ± 1 ns
fR (breaths minute)1) 15 ± 3 21 ± 3 20 ± 3 ns
PE¢CO2 (mmHg) 52 ± 1 47 ± 1 48 ± 1 10–30, 10–40
PE¢CO2 (kPa) 6.9 ± .01 6.3 ± 0.1 6.4 ± 0.1
PaCO2 (mmHg) 51.7 ± 0.7 51.6 ± 0.7 51.5 ± 0.7 ns
PaCO2 (kPa) 6.9 ± .01 6.9 ± 0.1 6.9 ± 0.1
V_ D (%) 0.0 ± 2.4 8.0 ± 2.4 6.0 ± 2.4 10–30
PaO2 (mmHg) 163.8 ± 14.3 143.3 ± 14.2 136.5 ± 14.2 10–30, 10–40
PaO2 (kPa) 21.8 ± 1.9 19.1 ± 1.9 18.2 ± 1.9
PaO2/FIO2 294.3 ± 25.3 269.9 ± 24.9 259.0 ± 25.3 ns
pHa 7.42 ± 0.006 7.43 ± 0.006 7.44 ± 0.006 10–40
HCO3) (mmol L)1) 33.5 ± 0.5 34.7 ± 0.5 35.4 ± 0.5 10–30, 10–40
Base Excess (mmol L)1) 8.5 ± 0.5 9.5 ± 0.5 10.2 ± 0.5 10–30, 10–40

All values are presented as least square means ± SE.

ns, nonsignificant.
*Values for one foal were excluded for the 10-minute reading as the nasal oxygen was not given for the first 15 minutes of the study.

limitation, shunt, or V/ _ mismatch. Although

_ Q
diffusion limitations cannot be excluded as a cause
for the decrease in PaO2, all foals in this study were
young and deemed to be healthy based on history
and physical examination findings. Mild hypoven-
tilation was documented in the foals before they
were hoisted, however, PaCO2 was unchanged
after hoisting. The observed increase in estimated
fraction of alveolar dead space ventilation and
decrease in the PaO2/FIO2 ratio documented in
these foals indicate that hoisting exacerbated the
_ Q
V/ _ mismatch and, consequently, the PaO2
decreased (Severinghaus & Stupfel 1957; Covelli
et al. 1983; Hardman & Aitkenhead 1999; West
2005).
Conflicting results have been reported on the
impact of lateral recumbency on PaO2. The right
lung lobe of the horse is anatomically larger than the
left one, which fact has been used to explain changes
in blood gases with higher PaO2 values and less
ventilation–perfusion impairment for horses lying
in left rather than in right lateral recumbency
(McDonell et al. 1979; Hornof et al. 1986).
Confounding observations were made by Day et al.
(1995) by documenting higher PaO2 values in
horses lying on their right sides compared with their
left. The differences were statistically significant but
the authors proposed that the difference would not
be of clinical significance. In another investigation,
no significant differences in PaO2 between right or
left lateral recumbency were measured in spontane-
ously breathing, halothane-anesthetized horses that
were turned into lateral position after 45 minutes of
dorsal recumbency (Gleed & Dobson 1988). To avoid
the potential influence of initial lateral recumbency
on our results, half of the foals were placed in left and
the other half were placed in right lateral recum-
bency. No significant differences were measured
between the positions.
The foals breathed room-air supplemented with
oxygen during anesthesia and, despite mild hypo-
ventilation (mean PaCO2 52 mmHg), maintained
PaO2 values above those measured in conscious
horses breathing room-air. These values were less
than expected for breathing approximately 54%
inspired oxygen, reflected in the relatively low
PaO2/FIO2 ratios. This may have been as result of
the accumulation of oxygen in the endotracheal
tube at the beginning of each breath and therefore
artificially increased FIO2 values may have been

22  2009 University of Georgia, 36, 18–24

 Hoisting decreased PaO2 in anesthetized horses C Braun et al.
measured. The theoretical calculation of tidal vol-
ume, inspiratory time, and flow rate suggests that
FIO2 would be closer to 0.35. Nevertheless, this
should not alter the measured trend of these values.
Ideally an inspiratory waveform monitor should
have been used to ensure more accurate measure-
ments of FIO2.
Oxygen administration at 15 L minute)1 has
been recommended for adult horses by intranasal
or tracheal insufflation during recovery from gen-
eral anesthesia to prevent hypoxemia (Moore et al.
1978; McMurphy & Cribb 1989) as 10 L minute)1
oxygen has been determined insufficient (Mason
et al. 1987). As the foals in this investigation had an
average body weight of only 223 ± 47 kg low PaO2
values were not expected at an O2 flow of 15 L min-
ute)1. The PaO2/FIO2 ratio was chosen to adjust for
variable FIO2 in individual animals. Investigations
of the effect of inspired oxygen concentrations on
pulmonary function have described an increase in
PaO2 in anesthetized horses in dorsal recumbency
breathing 100% oxygen versus 50% oxygen and
50% nitrogen (Gleed & Dobson 1988), and an
increase in PaO2 and shunt fraction in horses
breathing 100% oxygen (Marntell et al. 2005b), but
no change in shunt fraction with 30% inspired
oxygen compared with air in humans (Rothen et al.
1995).
Heart rates and AP values were consistent with
values previously reported for the anesthetic com-
bination. Mean arterial pressure progressively
decreased over 40 minutes of anesthesia to an
average of 99 ± 4 mmHg. Although the decrease
was statistically significant, none of the foals was
hypotensive. This trend is similar to measurements
recorded in ponies anesthetized with GKX (Greene
et al. 1986). Arterial blood pressure was not
decreased 5 minutes after hoisting in the foals in
this study. However, a sudden decrease at the
beginning of hoisting with a fast recovery was
observed in a few foals where it was possible to
maintain the blood pressure transducer in place
during hoisting.
A minimum of 75 minutes elapsed between
administration of xylazine for jugular catheter
placement and start of the experiment in 10 foals;
the time lapse was 30 minutes for one foal and for
another the time of xylazine administration was not
recorded. Administration of xylazine, 1.1 mg kg)1
IV, in horses causes significant decreases in heart
rate, cardiac output, and respiratory frequency, and
increased AP initially followed by a decrease (Muir
 2009 University of Georgia, 36, 18–24
et al. 1979; Lavoie et al. 1992; Moore & Trim 1992;
Yamashita et al. 2000). Arterial PO2 has been
documented to decrease (Lavoie et al. 1992) or
remain unchanged (Muir et al. 1979; Moore & Trim
1992; Yamashita et al. 2000). The duration of
significant effects is from 10 to 30 minutes with a
progressive change toward pre-administration val-
ues over 60–80 minutes. Effects of xylazine admin-
istration are dose-dependent and the dose of
xylazine given for jugular vein catheterization
before anesthesia was approximately one-third of
that used for pre-medication. Nonetheless, it is
possible that this administration of xylazine could
have influenced the cardiopulmonary effects of
anesthesia in some foals.
All animals were standing in <61 minutes after
discontinuing anesthesia. Eleven of 12 recoveries
were scored good to excellent and one foal, that
remained recumbent for 56 minutes and then made
multiple attempts to rise until standing 5 minutes
later, was scored as having an adequate recovery.
Satisfactory recoveries are expected from GKX
anesthesia of <90 minutes duration (Young et al.
1993).
Conclusion
The results of this study confirm that hoisting
healthy foals into dorsal recumbency during
injectable anesthesia decreases PaO2. Administra-
tion of supplemental oxygen during anesthesia and
recovery, and close monitoring are prudent prac-
tices to prevent or identify major abnormalities. The
extent to which hoisting for transportation of
anesthetized horses influences the anesthetic epi-
sode and recovery of horses needs further investi-
gation by comparison with alternative methods of
management such as table induction or rolling
tables.
Acknowledgements
The authors thank Dr Gary Huesner, Department of
Animal & Dairy Science, College of Agriculture &
Environmental Sciences, University of Georgia, for
his assistance.
References
Covelli HD, Nessan VJ, Tuttle WK III (1983) Oxygen
derived variables in acute respiratory failure. Crit Care
Med 11, 646–649.
23
Hoisting decreased PaO2 in anesthetized horses C Braun et al.
Cuvelliez S, Rosseel G, Blais D et al. (1995) Intravenous
anesthesia in the horse: comparison of xylazine–keta-
mine and xylazine–tiletamine–zolazepam combinations.
Can Vet J 36, 613–618.
Day TK, Gaynor JS, Muir WW III et al. (1995) Blood gas
values during intermittent positive pressure ventilation
and spontaneous ventilation in 160 anesthetized horses
positioned in lateral or dorsal recumbency. Vet Surg 24,
266–276.
Ellis RG, Lowe JE, Schwark WS, Taylor JI (1977) Intra-
venously administered xylazine and ketamine HCl
for anesthesia in horses. J Equine Med Surg 1, 259–265.
Gasthuys F, de Moor A, Parmentier D (1991) Haemo-
dynamic effects of change in position and respiration
mode during a standard halothane anaesthesia in
ponies. Zentralbl Veterinarmed A 38, 203–211.
Gleed RD, Dobson A (1988) Improvement in arterial
oxygen tension with change in posture in anaesthetised
horses. Res Vet Sci 44, 255–259.
Greene SA, Thurmon JC, Tranquilli WJ et al. (1986) Car-
diopulmonary effects of continuous intravenous infusion
of guaifenesin, ketamine, and xylazine in ponies. Am J
Vet Res 47, 2364–2367.
Hardman JG, Aitkenhead AR (1999) Estimation of alveolar
deadspace fraction using arterial and end-tidal CO2: a
factor analysis using physiological simulation. Anaesth
Intensive Care 27, 452–458.
Hall LW, Gillespie JR, Tyler WS (1968) Alveolar–arterial
oxygen tension differences in anaesthetized horses. Br J
Anaesth 40, 560–568.
Hall LW (1979) Oxygenation of pulmonary vein blood in
conscious and anaesthetised ponies. Equine Vet J 11,
71–75.
Hornof WJ, Dunlop CI, Prestage R et al. (1986) Effects of
lateral recumbency on regional lung function in anes-
thetized horses. Am J Vet Res 47, 277–282.
Hubbell JA, Bednarski RM, Muir WW (1989) Xylazine and
tiletamine–zolazepam anesthesia in horses. Am J Vet Res
50, 737–742.
Lavoie JP, Pascoe JR, Kurpershoek CJ (1992) Effects of
xylazine on ventilation in horses. Am J Vet Res 53, 916–
920.
Marntell S, Nyman G, Funkquist P et al. (2005a) Effects of
acepromazine on pulmonary gas exchange and circu-
lation during sedation and dissociative anaesthesia in
horses. Vet Anaesth Analg 32, 83–93.
Marntell S, Nyman G, Hedenstierna G (2005b) High
inspired oxygen concentrations increase intrapulmo-
nary shunt in anaesthetized horses. Vet Anaesth Analg
32, 338–347.
Mason DE, Muir WW, Wade A (1987) Arterial blood gas
tensions in the horse during recovery from anesthesia.
J Am Vet Med Assoc 190, 989–994.
McDonell WN, Hall LW, Jeffcott LB (1979) Radiographic
evidence of impaired pulmonary function in laterally
recumbent anaesthetised horses. Equine Vet J 11, 24–32.
24
McMurphy RM, Cribb PH (1989) Alleviation of postanes-
thetic hypoxemia in the horse. Can Vet J 30, 37–41.
Moore JN, Garner HE, Johnson JH et al. (1978) Continuous
administration of oxygen during the immediate pos-
tanesthetic period. Vet Med Small Anim Clin 73, 1397–
1398.
Moore RM, Trim CM (1992) Effect of xylazine on cere-
brospinal fluid pressure in conscious horses. Am J Vet
Res 53, 1558–1561.
Muir WW, Skarda RT, Sheehan W (1978) Evaluation of
xylazine, guaifenesin and ketamine hydrochloride for
restraint in horses. Am J Vet Res 39, 1274–1278.
Muir WW, Skarda RT, Sheehan W (1979) Hemodynamic
and respiratory effects of a xylazine–acetylpromazine
drug combination in horses. Am J Vet Res 40, 1518–
1522.
Muir WW 3rd, Mason DE (1993) Effects of diazepam,
acepromazine, detomidine and xylazine on thiamylal
anesthesia in horses. J Am Vet Med Assoc 203, 1031–
1038.
Nyman G, Hedenstierna G (1989) Ventilation–perfusion
relationships in the anaesthetised horse. Equine Vet J
21, 274–281.
Nyman G, Funkquist B, Kvart C et al. (1990) Atelectasis
causes gas exchange impairment in the anaesthetised
horse. Equine Vet J 22, 317–324.
Rothen HU, Sporre B, Engberg G et al. (1995) Reexpansion
of atelectasis during general anaesthesia may have a
prolonged effect. Acta Anaesthesiol Scand 39, 118–125.
Schatzmann U, Koehli M, Dudan F et al. (1982) Effect of
postural changes on certain circulatory and respiratory
values in the horse. Am J Vet Res 43, 1003–1005.
Severinghaus JW, Stupfel M (1957) Alveolar dead space as
an index of distribution of blood flow in pulmonary
capillaries. J Appl Physiol 10, 335–348.
Sorenson PR, Robinson NE (1980) Postural effects on lung
volumes and asynchronous ventilation in anesthetized
horses. J Appl Physiol 48, 97–103.
Stegmann GF, Littlejohn A (1987) The effect of lateral and
dorsal recumbency on cardiopulmonary function in the
anaesthetised horse. J S Afr Vet Assoc 58, 21–27.
Wan PY, Trim CM, Mueller PO (1992) Xylazine–ketamine
and detomidine–tiletamine–zolazepam anesthesia in
horses. Vet Surg 21, 312–318.
West JB (2005) Respiratory Physiology – The Essentials.
(7th edn), Lippincott Williams & Wilkins, Philadelphia,
PA, pp. 67–72.
Yamashita K, Tsubakishita S, Futaok S et al. (2000)
Cardiovascular effects of medetomidine, detomidine
and xylazine in horses. J Vet Med Sci 62, 1025–1032.
Young LE, Bartram DH, Diamond MJ et al. (1993) Clinical
evaluation of an infusion of xylazine, guaifenesin and
ketamine for maintenance of anaesthesia in horses.
Equine Vet J 25, 115–119.
Received 11 September 2007; accepted 25 January 2008.
 2009 University of Georgia, 36, 18–24