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S E CT I O N III RECENT ADVANCES IN ANESTHESIA
Jörg A. Auer
CHAPTER 19
Advances in
Inhalation Anesthesia
Alexander Valverde
Inhalation anesthesia is a versatile technique that facilitates
many different types of surgical and diagnostic procedures
in the equine patient, ranging from short to long, from
elective to emergency, and from routine to complicated.
Halothane and methoxyflurane were introduced into
clinical anesthetic practice in the early 1960s and their use
became widespread in veterinary medicine. Methoxyflurane
is no longer available because of the advent of novel
inhalation anesthetics such as isoflurane (in the late 1970s)
and more recently, sevoflurane and desflurane (in the
1990s). Halothane is also slowly disappearing from daily
use in North America, although it continues to be widely
used in Europe.
Novel drugs should provide significant advantages over
previously used drugs if they are to replace them.
Advantages of novel inhalation anesthetics should include
less morbidity and mortality, better and more rapid control
of anesthetic depth, less cardiorespiratory depression, and
less biotransformation.
ANESTHETIC RISK
“A chance to cut is a chance to kill.”
G. Mark Johnson1
Complications arising from general anesthesia are common.
Not all recognized complications reflect an immediate
danger to the patient; however, identifying their significance
and addressing them promptly may reduce their impact.
Because most surgery is performed under general anesthesia,
deaths during that time have been coined “anesthetic
deaths.” Some deaths can be considered as inevitable—for
example, after rupture of major vessels. In addition, cardiac
arrest can be a nonanesthetic event related to direct surgical
complications, or it could be part of an anaphylactic reac-
tion. Thus, not all causes of death are directly related to
anesthesia. The most common causes of cardiac arrest
associated with anesthesia include hypoxia because of
ventilatory problems, drug overdose, and perioperative
hypotension.
The anesthetic death rate in humans has decreased from
1 death per 2700 anesthesias in the 1950s,2 to 1 in 4761 in
the 1970s, and to 1 in 10,000 in the 1980s.3 Anesthetic deaths
have decreased over the years probably as a result of safer
anesthetic drugs, better techniques, and more sophisticated
monitoring and support equipment that allow early detec-
tion of problems and intervention. On the other hand, for
these same reasons, it is now common to perform surgery or
diagnostic procedures on critically ill patients, which con-
tribute to the overall mortality rate despite recent anesthetic
advances.
Equine studies have reported a death rate of 1 per 1250
anesthesias for elective procedures when only anesthetic
causes are considered. Mortality increases to 1 in 158 cases
when anesthetic and surgical causes, such as bleeding in the
immediate postoperative period, fractured limbs during
recovery, and shock, are included.4 If the entire hospi-
talization period from the time of anesthesia until the final
outcome of the case is taken into account, then the overall
death rate may be as high as 1 in 28.4
Emergency cases had a higher overall death rate of 1 in
3.2 cases (1 in 2.8 for colic and 1 in 6.5 for noncolic cases)
than elective cases when the entire hospitalization period
is taken into account.5 Surgical and/or anesthetic deaths
represented 1 in 23 cases in the colic group and 1 in 50
cases in the noncolic group if only the immediate post-
operative period is considered.5 From these two studies,4,5
risk of death is 4.25 times more likely for emergency pro-
cedures not associated with colic than for similar procedures
carried out electively. Emergency general anesthesia for
colic carries an increased risk of death 9.86 times that of
elective cases.5 These numbers are worrisome, but they
include death by euthanasia, and that decision is influenced
by many factors, including financial and prognosis for
athletic future.
Morbidity and mortality studies are necessary to deter-
mine if one anesthetic drug or technique can positively
influence outcome. However, these studies are difficult to
design and execute because of the multiple factors involved.
In an effort to identify drugs and techniques that may be
linked to anesthetic death in horses, a confidential enquiry
into perioperative equine fatalities (CEPEF) analyzed data
from over 40,000 anesthetic records.6
Findings from the CEPEF study identified an increased
risk of death associated with techniques that involved an
inhalation anesthetic only as part of the induction tech-
nique, a common practice in neonatal foals.6 Tachypnea and
release of catecholamines have been suggested as possible
causes that predispose to anesthetic overdose in foals, as
well as increased overall requirement for the inhalation
anesthetic because premedicant and induction agents are
not used.6 Age was also linked to anesthetic death rate,
which was highest in the very young, followed by the older
horse, and lowest in young adults.6
219
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220 RECENT ADVANCES IN ANESTHESIA
Maintenance of anesthesia with inhalation anesthetics
carried a threefold higher risk of death than injectable anes-
thetics.6 Improved outcome with injectable anesthetics may
reflect their use for shorter anesthetic procedures, as risk of
death also increases with duration of anesthesia and surgery
time, a situation in which injectable techniques are less
likely to be used.6,7 In addition, intravenous anesthetics
cause less cardiovascular depression than inhalation anes-
thetics.8 Most of the anesthetic deaths were related to cardiac
arrest (33%),6 which explains the association between
inhalation anesthetics and mortality. Of all anesthetic drugs
and protocols used in over 35,400 cases, inhalation anes-
thetics were used as the maintenance agent in 87%, and
injectables or no additional anesthetic were used for the
remaining 13%.6 Despite the higher risk involved with
inhalation anesthetics, the ease of administration with appro-
priate equipment and the ability to alter anesthetic depth
makes them the most common method of maintaining
anesthesia in equine patients at this time.
In the study by Johnston and colleagues,6 most of the
horses under inhalation anesthesia received halothane
(98%) versus isoflurane (2%), and it is unclear whether
overall mortality from inhalation anesthetics can be gen-
eralized to both drugs. The death rate for halothane was 1
death per 101 cases and 1 in 78 cases for isoflurane, whereas
for injectable agents it was 1 in 321 cases.6
In a randomized prospective study that included elective
and emergency cases from several equine clinics around
the world, and with approximately 4100 horses receiving
halothane and a similar number isoflurane, comparisons
of mortality were similar; 1.7% versus 1.6%, respectively.9
The only difference between the two inhalants was demon-
strated in horses 2 to 5 years of age, where the use of
isoflurane reduced the death rate fivefold.9 The main causes
of death in this study were cardiac arrest (32%) and fractures
(23%).9 Isoflurane use was associated with less risk of
cardiac-related mortality than halothane (30% versus 70%
of cardiac deaths, respectively).9 Fractures may be related
to poor perfusion to muscle groups secondary to cardio-
vascular depression and the subsequent myopathy that
manifests in the recovery period. However, there were no
significant differences between isoflurane and halothane
in respect to myopathy.9 Duration of anesthesia (over
90 minutes) and lateral recumbency were the two factors
that carried an increased risk of myopathy in this study.9
Despite the lack of evidence for advantages of isoflurane
over halothane, it is generally agreed that isoflurane and
novel inhalant anesthetics (sevoflurane and desflurane)
depress myocardial function and cardiac output less than
halothane10-15 and should be selected in more critical cases
when perfusion and oxygenation may be impaired.
ANESTHETIC DEPTH
The novel inhalation anesthetics such as isoflurane, sevoflu-
rane, and desflurane are less potent and less soluble than
older agents such as halothane (Table 19-1). Potency is
indicated by the minimum alveolar concentration (MAC),
defined as the alveolar concentration of inhalation anes-
thetic that prevents movement in 50% of subjects in
response to a noxious stimulus. Thus, the MAC of novel
drugs is higher than that of the older drugs.
TABLE 19-1. Minimum Alveolar Concentration (MAC)
and Blood/Gas Partition Coefficient Values of
Inhalant Anesthetics in the Horse
Blood/Gas*
MAC (%) Humans Horse35
Halothane 0.82-0.9536-39 2.4 1.66
39
Isoflurane 1.31 1.4 0.92
Sevoflurane 2.3140 0.6 0.47
Desflurane 7.6 41
0.42 ND
*These values are significantly lower in horses than for people.
The low lipid solubility (expressed as the blood/gas
partition coefficient) of novel anesthetics is responsible
for their lower potency because a higher concentration is
required to achieve equilibrium between the two compart-
ments (blood and alveoli) (see Table 19-1). The concen-
tration of anesthetic in the alveoli is a reflection of the brain
concentration for that particular drug. By controlling the
concentration in the alveoli, with minimal impact from the
lipid solubility of the drug in other tissues, changes in
anesthetic plane can be achieved more readily and result in
faster onset or disappearance of clinical effects.
In horses, a faster recovery is advantageous only if the
animal has fully regained mental and motor function. The
unique behavior of the horse compels it to assume a
standing position early in the recovery period, and pre-
mature attempts to stand may result in a stormy recovery
and major injuries. In the recovery period, horses attempt to
move and change body position even when end-tidal
anesthetic concentrations sufficient for clinical planes of
anesthesia are still measurable.16 The administration of
sedative drugs, including alpha-2 agonists, during this time
has been advocated to prevent early movement attempts and
improve the quality of recovery.17
Duration of anesthesia also influences the quality of recov-
ery. Isoflurane results in faster, but often less controlled,
recoveries than halothane in horses anesthetized for periods
of less than 2 hours.11,13,18 In horses anesthetized for periods
of 3 hours or longer, the recoveries were better with isoflu-
rane, as horses appeared more alert and less ataxic than after
halothane.16 The solubility of halothane may account for
more accumulation after a prolonged anesthetic delivery. In
contrast, horses recovering from 1 hour of halothane anes-
thesia tended to have more ideal recoveries than horses recov-
ering from 3 hours of halothane or isoflurane anesthesia.16
Sevoflurane results in more controlled recoveries than
isoflurane, although no differences in times to standing were
demonstrated between the two drugs. The better recoveries
after sevoflurane may be the result of its lower solubility.11 In
foals less than 3 months of age, no differences were detected
in the induction or recovery times and quality scores
between sevoflurane and isoflurane; however, these foals
were assisted during recovery.13
CARDIORESPIRATORY EFFECTS
In general, cardiovascular depression from inhalant anes-
thetics is dose dependent. Normally expressed as MAC
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ADVANCES IN INHALATION ANESTHESIA
multiples for the specific inhalant, the higher the MAC mul-
tiple delivered to the patient, the more pronounced was the
cardiovascular depression. Using MAC multiples allows
comparison of different inhalant anesthetics, based on the
principle that there is equipotency between them at the
same MAC level.
The cardiovascular effects of inhalant anesthetics can be
divided into those that occur under mechanical ventilation
and those under spontaneous ventilation. Dose-dependent
decreases in cardiac output, stroke volume, and blood pres-
sure are common with all inhalant anesthetics. However,
these parameters are better maintained during spontaneous
than during controlled ventilation because of the stimu-
latory effects of arterial CO2, which is higher during
spontaneous breathing.10,19,20 In addition, changes in
intrathoracic pressure that occur in ventilated horses have a
negative effect on venous return that further depresses
cardiac function.10,20
Cardiac output, blood pressure, and systemic vascular
resistance increased significantly from baseline in horses
anesthetized with isoflurane during volume-controlled
ventilation that allowed arterial CO2 tensions to increase to
moderate levels (PaCO2 of 75 to 85 mm Hg) from normal
values (35 to 45 mm Hg). In this same study, mild hyper-
capnia (55 to 65 mm Hg) caused only a minor decrease in
cardiac output and an increase in vascular resistance.19
In horses breathing spontaneously, cardiovascular
variables were similar between isoflurane and halothane
MAC multiples in one study,10 and they were less depressed
by isoflurane and sevoflurane than halothane in another.11
Under controlled ventilation, isoflurane caused less depres-
sion of cardiac output and stroke volume than halothane,
and similar changes in blood pressure, but vascular periph-
eral resistance was decreased with isoflurane more than with
halothane.10 Similar findings of better cardiovascular func-
tion with isoflurane compared with halothane have been
described in horses anesthetized under hypoxemic condi-
tions (PaO2 of 50 mm Hg) for 3 hours.15
Changes in cardiac output, blood pressure, and periph-
eral vascular resistance are similar with isoflurane and with
sevoflurane at 1.5 MAC, which represents a moderate plane
of surgical anesthesia.11 Similarly, in foals anesthetized for
approximately 1 hour, no differences between sevoflurane
and isoflurane were detected in cardiovascular effects.13
Desflurane causes cardiovascular changes similar to those
caused by isoflurane and sevoflurane; it decreases vascular
resistance and blood pressure, whereas cardiac output and
heart rate remained unchanged at 1 MAC.14
Halothane causes a decrease in blood pressure that is
more related to a decrease in myocardial contractility and
cardiac output than to a decrease in peripheral resistance.
On the other hand, isoflurane, sevoflurane, and desflurane
lower blood pressure as a result of decreased peripheral
resistance and tend to cause less depression of cardiac out-
put and contractility. Based on these findings, isoflurane,
sevoflurane, and probably desflurane provide better tissue
flow both in foals and adult horses and therefore may be
safer, especially in the critically ill patient.
No major differences in heart rate are observed between
isoflurane, sevoflurane, and halothane.11 The arrhythmo-
genicity of halothane in response to doses of epinephrine is
also higher than for isoflurane, sevoflurane, or desflurane.21-23
221
Halothane-anesthetized horses breathe at a faster rate
than horses on isoflurane. Respiratory rate also decreases
progressively with increasing doses of isoflurane or sevoflu-
rane but not with halothane.10,11 Despite these differences,
PaCO2 tends to be similar with all inhalant anesthetics,
indicating similar minute-ventilation with all of them, most
probably as a result of an increased tidal volume in horses
receiving isoflurane or sevoflurane, to compensate for the
slower respiratory rate and a smaller tidal volume in horses
receiving halothane.
In spontaneously breathing anesthetized horses, respira-
tory rate is decreased to a similar extent by isoflurane,
sevoflurane, and desflurane and less by halothane.11,14 The
decrease in rate was accompanied by concomitant increases
in PaCO2.11
BIOTRANSFORMATION
Respiration is responsible for eliminating most inhalation
anesthetics. Liver metabolism is responsible for almost all
degradation of inhalation anesthetics that remain in the
body, although the lungs, kidneys, and other organs may
contribute to overall elimination.
Halothane is the only currently used inhalant anesthetic
that undergoes extensive metabolism (up to 20%) by the
liver. In comparison, isoflurane, sevoflurane, and desflurane
are metabolized to a much lesser extent (0.2%, 3% to 5%,
and 0.02%, respectively).24
The effects of inhalant anesthetics on hepatic blood flow
and metabolism should be minimal so that hepatic function
is sustained and toxicity problems are avoided. In animal
studies that have included dogs, rats, and pigs, the novel
inhalant anesthetics including isoflurane, sevoflurane, and
desflurane preserve hepatic metabolism and splanchnic
blood flow better than halothane.25-28 Similarly, in humans,
all three of the novel anesthetics are preferred over
halothane in patients with liver disease.29
Research horses anesthetized for up to 5 hours with only
halothane and maintained at 1 to 2 MAC during this time
exhibited a significant increase from baseline in aspartate
aminotransferase, lactate dehydrogenase, creatinine phos-
phokinase, and total bilirubin for up to 4 days after
anesthesia.30 Similar changes are observed, although sig-
nificantly less pronounced, when anesthesia time with
halothane is less than 2 hours in clinical cases.30 In contrast,
horses exposed to isoflurane for 5 hours at 1 to 2 MAC did
not exhibit significant changes in their serum chemistry
values.31 In a subsequent study, the same authors demon-
strated that increasing anesthetic time with halothane
beyond 5 hours increases the magnitude and duration of
these changes, suggesting liver dysfunction.32 Hepatic dys-
function in horses has been associated with halothane
anesthesia combined with hypoxemia, but not with isoflu-
rane and hypoxemia.15
Halothane has been implicated in cases of hepatic dys-
function in other species. Hepatic hypoxia with halothane is
reported to be a major cause of such changes because greater
reductions in hepatic blood flow occur with halothane than
with other inhalation anesthetics. In addition, the increased
biotransformation (20%) in the presence of reduced blood
flow and oxygenation will promote a reduction of metab-
olism. As mentioned before, only halothane undergoes this
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222 RECENT ADVANCES IN ANESTHESIA
type of metabolism. However, a reduction of metabolism
is not always linked directly to hepatotoxicity, as hepatic
damage also occurs with other anesthetics.33
GENERAL RECOMMENDATIONS
The transition from induction of anesthesia with injectable
agents to inhalation anesthesia, and then to emergence
from inhalation anesthesia, should be smooth. The use of
injectable drugs with sedative or anesthetic properties is
advised, especially in the neonate, as shown by mortality
studies.
High oxygen flows should be used in the first 10 to 15
minutes of anesthesia to carry the inhalation anesthetic into
the circuit and overcome the dilution effects of the anes-
thetic equipment (canister, reservoir bag, and breathing
circuit), the horse’s tidal volume and concentration gradi-
ents. In the adult horse, oxygen flows of 20 mL/kg per
minute are normally used during the first part of anesthesia
and then lowered to 10 mL/kg per minute for the remainder
of the anesthetic period. In foals, flows of 40 to 60 mL/kg
per minute are adequate, and this has less impact on cost
and allows the use of small animal anesthetic machines.
Carbon dioxide absorbers should be monitored and
changed regularly, usually after 5 to 7 hours of use at the
oxygen flow rates just described. This also prevents accu-
mulation of carbon monoxide, which may occur especially
with desflurane, isoflurane, and halothane when low oxygen
flows are used and soda lime is the choice of carbon dioxide
absorbent. Production of compound A from sevoflurane in
the presence of barium lime, and to a lesser degree with soda
lime, can occur when low oxygen flows are used. This com-
pound is reported to be nephrotoxic in rats,34 and although
similar data are not available in horses, caution is advised.
In conclusion, novel inhalation anesthetics with lower
blood/gas partition coefficients have been introduced over
the last 40 years. The advantages of these drugs are less
biotransformation, less cardiovascular depression, and more
rapid changes in anesthetic depth. Isoflurane, sevoflurane,
and desflurane are drugs with similar anesthetic effects in
the horse and the choice of agent depends on personal
preference, available vaporizers, and financial considera-
tions. Whether the novel agents will result in lower fatality
rates remains to be seen.
REFERENCES
1. Johnston GM: Equine anaesthesia: A chance to cut is a chance to
kill, Proc Assoc Vet Anaesth 2000:1-2.
2. Beecher HK, Todd DP: A study of the deaths associated with anes-
thesia and surgery: Based on a study of 599,548 anesthesias in ten
institutions 1948-1952, inclusive, Ann Surg 1954;140:2.
3. Keenan RL, Boyan CP: Decreasing frequency of anesthetic cardiac
arrests, Clin Anesth 1991;3:354.
4. Mee AM, Cripps PJ, Jones RS: A retrospective study of mortality
associated with general anaesthesia in horses: Elective procedures,
Vet Rec 1998;142:275.
5. Mee AM, Cripps PJ, Jones RS: A retrospective study of mortality
associated with general anaesthesia in horses: Emergency pro-
cedures, Vet Rec 1998;142:307.
6. Johnston GM, Eastment JK, Wood JLN, et al: The confidential
enquiry into perioperative equine fatalities (CEPEF): mortality
results of Phases 1 and 2, Vet Anaesth Analg 2002;29:159.
7. Johnston GM, Taylor PM, Holmes MA, et al: Confidential enquiry
of perioperative equine fatalities (CEPEF-1): Preliminary results,
Equine Vet J 1995;27:193.
8. Taylor PM, Kirby JJ, Shrimpton DJ, et al: Cardiovascular effects of
surgical castration during anesthesia maintained with halothane or
infusion of detomidine, ketamine and guaiphenesin in ponies,
Equine Vet J 1998;30:304.
9. Johnston GM, Eastment JK, Taylor PM, et al: Is isoflurane safer
than halothane in equine anaesthesia? Results from a prospective
multicentre randomized controlled trial, Equine Vet J 2004;36:64.
10. Steffey EP, Howland D Jr: Comparison of circulatory and respi-
ratory effects of isoflurane and halothane anesthesia in horses, Am
J Vet Res 1980;41:821.
11. Grosenbaugh DA, Muir WW: Cardiorespiratory effects of sevoflu-
rane, isoflurane, and halothane anesthesia in horses, Am J Vet Res
1998;59:101.
12. Raisis AL, Young LE, Blissitt KJ, et al: A comparison of the haemo-
dynamic effects of isoflurane and halothane anaesthesia in horses,
Equine Vet J 2000;32:318.
13. Read MR, Read EK, Duke T, et al: Cardiopulmonary effects and
induction and recovery characteristics of isoflurane and sevoflurane
in foals, J Am Vet Med Assoc 2002;221:393.
14. Clarke KW, Song DY, Alibhai HI, et al: Cardiopulmonary effects of
desflurane in ponies, after induction of anaesthesia with xylazine
and ketamine, Vet Rec 1996;139:180.
15. Whitehair KJ, Steffey EP, Woliner MJ, et al: Effects of inhalation
anesthetic agents on response of horses to three hours of
hypoxemia, Am J Vet Res 1996;57:351.
16. Whitehair KJ, Steffey EP, Willits NH, et al: Recovery of horses from
inhalation anesthesia, Am J Vet Res 1993;54:1693.
17. Santos M, Fuente M, Garcia-Iturralde P, et al: Effects of alpha-2
adrenoceptor agonists during recovery from isoflurane anaesthesia
in horses, Equine Vet J 2003;35:170.
18. Donaldson LL, Dunlop GS, Holland MS, et al: The recovery of
horses from inhalant anesthesia: A comparison of halothane and
isoflurane, Vet Surg 2000;29:92.
19. Khanna AK, McDonell WN, Dyson DH, et al: Cardiopulmonary
effects of hypercapnia during controlled intermittent positive
pressure ventilation in the horse, Can J Vet Res 1995;59:213.
20. Hodgson DS, Steffey EP, Grandy JL, et al: Effects of spontaneous,
assisted and controlled ventilatory modes in halothane-anes-
thetized geldings, Am J Vet Res 1986;47:992.
21. Pettifer G, Dyson D, McDonell W: The arrhythmogenic dose of
epinephrine in halothane and isoflurane anesthetized dogs: An
assessment of repeatability, Can J Vet Res 1997;61:221.
22. Hikasa Y, Okabe C, Takase K, et al: Ventricular arrhythmogenic dose
of adrenaline during sevoflurane, isoflurane, and halothane
anaesthesia either with or without ketamine or thiopentone in cats,
Res Vet Sci 1996;60:134.
23. Moore MA, Weiskopf RB, Eger EI 2nd, et al: Arrhythmogenic doses
of epinephrine are similar during desflurane or isoflurane anes-
thesia in humans, Anesthesiology 1993;79:943.
24. Stoelting R: Pharmacology and Physiology in Anesthetic Practice,
ed 3, Philadelphia, 1999, Lippincott-Raven.
25. Debaene B, Goldfarb G, Braillon T, et al: Effects of ketamine,
halothane, enflurane and isoflurane on systemic and splanchnic
hemodynamics in normovolemic and hypovolemic cirrhotic rats,
Anesthesiology 1990;73:118.
26. Sugai M: Comparison of the effect of isoflurane and that of
sevoflurane on hepatic circulation and oxygen metabolism during
acute hypoxia in dogs, Masui 1996;45:608.
27. Bernard JM, Doursout MF, Wouters P, et al: Effects of sevoflurane
and isoflurane on hepatic circulation in the chronically instru-
mented dog, Anesthesiology 1992;77:541.
28. Armbruster K, Noldge-Schomburg GF, Dressler IM, et al: The effects
of desflurane on splanchnic hemodynamics and oxygenation in the
anesthetized pig, Anesth Analg 1997;84:271.
29. Green DW, Ashley EMC: The choice of inhalation anaesthetic for
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MODERN INJECTION ANESTHESIA
major abdominal surgery in children with liver disease, Paed
Anaesth 2002;12:665.
30. Steffey EP, Farver T, Zinkl J, et al: Alterations in horse blood cell
count and biochemical values after halothane anesthesia, Am J Vet
Res 1980;41:934.
31. Steffey EP, Zinkl J, Howland D Jr: Minimal changes in blood cell
counts and biochemical values associated with prolonged isoflu-
rane anesthesia of horses, Am J Vet Res 1979;40:1646.
32. Steffey EP, Giri SN, Dunlop CI, et al: Biochemical and haemato-
logical changes following prolonged halothane anaesthesia in
horses, Res Vet Sci 1993;55:338.
33. Shingu K, Eger EI, Johnson BH, et al: Hepatic injury induced by
anesthetic agents in rats, Anesth Analg 1983;62:10.
34. Keller K, Callan C, Prokocimer P, et al: Inhalation toxicology study
of a haloalkene degradant of sevoflurane, compound A (PIFE), in
Sprague Dawley rats, Anesthesiology 1995;83:1220.
35. Bergadano A, Lauber R, Zbinden A, et al: Blood/gas partition
coefficient of halothane, isoflurane and sevoflurane in horse blood,
Br J Anesth 2003;91:276.
CHAPTER 20
Modern Injection
Anesthesia for Horses
Regula Bettschart-Wolfensberger
The use of inhalational anesthesia is generally limited to
larger clinics because of equipment costs, the requirement
for an oxygen source, and the need for a scavenging system
for waste gases. There is also strong evidence that inhalant
techniques are associated with a higher mortality rate in
horses (see Chapter 19). Therefore, the use of safe intra-
venous anesthesia techniques in practice is both desirable
and advantageous. The most important features of intra-
venous protocols are a smooth, excitement-free induction
phase with a slow lowering of the body into sternal and
lateral recumbency, minimal cardiopulmonary depression,
and a calm recovery with a single attempt to stand and
minimal ataxia. Other factors include good muscle relaxa-
tion and analgesia, as well as the possibility to assess depth
of anesthesia and modify depth and duration of anesthesia
in a quick and predictable manner.
Injectable anesthetic combinations are presently used for
anesthesia induction and for short (up to 30 minutes),
minor surgical procedures. Longer surgeries are performed
with intravenous anesthesia induction followed by inhala-
tion, or less commonly by total intravenous anesthesia
(TIVA). Features of short-duration injection anesthesia are
discussed separately from long-duration (anesthetic dura-
tion over 30 minutes) TIVA. Anesthetics discussed in this
chapter include ketamine and propofol and useful combi-
nations of these two drugs. Older agents such as barbitu-
rates, chloral hydrate, and drugs suitable for the anesthesia of
223
36. Doherty TJ, Frazier DL: Effect of intravenous lidocaine on
halothane minimum alveolar concentration in ponies, Equine Vet
J 1998;30:300.
37. Doherty TJ, Geiser DR, Rohrbach BW: Effect of acepromazine and
butorphanol on halothane minimum alveolar concentration in
ponies, Equine Vet J 1997;29:374.
38. Doherty TJ, Geiser DR, Rohrbach BW: Effect of high volume
epidural morphine, ketamine and butorphanol on halothane
minimum alveolar concentration in ponies, Equine Vet J
1997;29:370.
39. Steffey EP, Howland D Jr, Giri S, et al: Enflurane, halothane, and
isoflurane potency in horses, Am J Vet Res 1977;38:1037.
40. Aida H, Mizuno Y, Hobo S, et al: Determination of the minimum
alveolar concentration (MAC) and physical response to sevoflurane
inhalation in horses, J Vet Med Sci 1994;56:1161.
41. Tendillo FJ, Mascias A, Santos M, et al: Anesthetic potency of
desflurane in the horse: Determination of the minimum alveolar
concentration, Vet Surg 1997;26:354.
wild Equidae, such as Immobilon (etorphine-acepromazine),
will not be discussed.
SHORT-DURATION INJECTION ANESTHESIA
For anesthesia induction, ketamine, tiletamine/zolazepam,
or propofol can be used. Adult horses must be adequately
sedated before anesthesia induction with a calculated
dosage of the selected drug. Only in very young foals and
in recumbent, severely compromised horses can anesthesia
be induced with administration of an anesthetic to effect.
For compromised horses, a mixture of equal volumes of
diazepam (5 mg/mL) and ketamine (100 mg/mL) is a safe
method for anesthesia induction and usually requires
1 mL/25 kg of the mixture (0.1 mg/kg diazepam + 2 mg/kg
ketamine). This protocol avoids the cardiovascular-
compromising side effects of α2-agonists. In foals, the
administration of propofol to effect is an alternative (see
Chapter 21).
Ketamine
Ketamine is the most widely used drug for anesthesia induc-
tion in horses. It provides good, mainly somatic analgesia
without inducing hypnosis. However, it is not suitable as a
sole agent, as it may cause seizure-like activity and muscle
rigidity. Appropriate sedation with α2-agonists or acepro-
mazine prior to induction is very important.1-14 The
additional use of drugs such as guaifenesin or benzo-
diazepines (diazepam or midazolam) will further improve
muscle relaxation.15-20 Guaifenesin is a safe drug with mini-
mal side effects at clinical dosages. It should be used as a
5% (50 mg/mL) solution, because higher concentrations
are associated with significant irritation of the veins21 and
intravenous hemolysis.
Guaifenesin is administered to the sedated horse to effect
(preferably under pressure, as effective dosages are large—
often 50 mg/kg, or 500 mL for a 500-kg horse). When
the horse begins to buckle at the knees, the induction
drug, most commonly ketamine (2 mg/kg), should be
given.