V 20TH ANNIVERSARY
9 September 1999
CE Refereed Peer Review
FOCAL POINT
★ All types of anesthetics can be
used in trauma patients, although
dosage requirements are reduced
and particular attention must be
paid to the traumatized organ
systems and potential adverse
effects of the chosen agent.
KEY FACTS
■ Anticholinergics, acepromazine,
and α2 agonists are generally
contraindicated in trauma
patients.
■ Opioids used alone
or in combination with
benzodiazepines can provide
excellent sedation and superior
analgesia, but respiratory
depression is a potential
complication.
■ With proper premedication,
etomidate is an ideal induction
agent, particularly for the
hemodynamically unstable
trauma patient; cost is its only
major drawback.
■ Isoflurane is the safest volatile
agent available for veterinary
use, although all such agents are
respiratory and cardiovascular
depressants.
Vol. 21, No.
Anesthetic Agents
in Trauma Patients
New England Veterinary Specialists, Brentwood, New Hampshire
Lee A. Garrod, DVM
Tufts University
Lois Wetmore, DVM
ABSTRACT: Trauma patients may require sedation or anesthesia for diagnostic procedures,
surgical procedures, or therapeutic intervention but may have injuries to the cardiovascular,
respiratory, or nervous systems. Some of the anesthetic agents available may be inappropriate
if they adversely affect systems already compromised in a patient. It is therefore important to
be familiar with the characteristics of the various classes of anesthetic agents. This article dis-
cusses the mechanisms of action, advantages, and disadvantages of certain anesthetic agents,
including anticholinergics, α2 adrenoreceptor agonists, phenothiazines, benzodiazepines, opi-
oids, barbiturates, propofol, etomidate, ketamine, neuromuscular blockers, and volatile anes-
thetics.
T
raumatic injury affects veterinary patients of all ages and is the leading
cause of death in dogs and cats younger than 3 years of age. Specific in-
juries must be identified and treated based on the potential risk of mor-
tality that they pose to the patient. Maintenance of a patent airway and intravas-
cular volume resuscitation are primary considerations.
Patients that present with major, multiple traumatic injuries may require seda-
tion, chemical restraint, or general anesthesia so that life-saving diagnostic and
therapeutic procedures can be performed. Such patients pose a tremendous chal-
lenge to veterinarians because most anesthetic agents (Table I) further depress
the cardiovascular and respiratory systems. This article discusses the anesthetic
and analgesic techniques and concerns unique to this population of patients.
ANESTHETIC REQUIREMENTS
There is no absolute anesthetic approach to trauma patients and no ideal anes-
thetic agent that provides analgesia and relaxation without depressing respiration
or compromising cardiovascular stability. Every effort should be made to stabi-
lize trauma patients before the induction of anesthesia. Only in unusual circum-
stances, such as continuing massive hemorrhage or closed head trauma with in-
tracranial hemorrhage, is it inadvisable to completely correct hypovolemia and
shock before surgical intervention.
Trauma patients are likely to have decreased anesthetic requirements and un-
predictable drug responses, particularly if they are hypovolemic or hypothermic.
Anesthetic drugs normally depress cardiovascular function and, in a patient that
Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE I
Anesthetic Agents, Routes of Administration, and Doses
Agent Dose (mg/kg) Advantages Disadvantages
Diazepam 0.2 IV Hemodynamic stability; reduce Propylene glycol carrier
Midazolam 0.2 IM or IV intracranial pressure in diazepam may cause
hypotension and bradycardia
with rapid IV administration

Morphine 0.5–1 IM or IV Cardiovascular stability; no Dose-dependent respiratory

Meperidine 1–2 IM (cats) effect on intracranial pressure; depression and bradycardia
Oxymorphone 0.05–0.2 IM or IV analgesia (varying potency);
Hydromorphone 0.05–0.2 IM or IV reversed with antagonist
Fentanyl 0.01–0.04 IM or IV
Butorphanol 0.2–0.4 SC, IM, or IV
Buprenorphine 0.01 IM or IV

Thiopental 10 IV Decreases intracranial pressure Myocardial depression;

arrhythmias; respiratory
depression

Ketamine 2–5 IV with diazepam Minimal cardiovascular Increases intracranial pressure

depression

Propofol 4–8 slow IV Ultrashort-acting; reduces Profound respiratory depression

0.2–0.3 mg/kg/min CRI intracranial pressure or apnea; hypotension; aseptic
handling; no analgesia

Etomidate 0.5–1 IV Very safe; ultrashort-acting; Very expensive; poor analgesia;

cardiovascular stability; no emesis and defecation on
respiratory depression induction and recovery unless
proper premedication

Succinylcholine 0.3–0.4 IV All but succinylcholine can be Patient must be intubated and
Pancuronium 0.02–0.06 IV partially reversed; little to no ventilated; increased intraocular
Atracurium 0.2–0.4 IV adverse side effects pressure with succinylcholine
Vecuronium 0.1 IV

Halothane To effect Isoflurane causes less cardiac Respiratory and myocardial

Isoflurane (1.5 MAC) depression than does halothane; depression; potential increase
rapid induction and recovery in intracranial pressure;
with isoflurane halothane arrhythmogenic as
it sensitizes the myocardium
to catecholamines
CRI = constant-rate infusion; IM = intramuscular; IV = intravenously; MAC = minimum alveolar concentration; SC = subcutaneously.

is already dehydrated and hypovolemic, can cause se-
vere hypotension.1 As a result, the initial dose of any
anesthetic agent used should be halved and subsequent-
ly titrated to effect. Premedication may not be neces-
sary in some patients. Agents administered subcuta-
neously or intramuscularly are likely to be poorly
absorbed in hypovolemic patients.
Trauma patients are susceptible to arrhythmias
caused by hypoxia (including pulmonary contusions,
pneumothorax, and pleural or pericardial effusions),
myocardial contusions from blunt chest trauma, en-
dogenous catecholamine release, hypothermia, and pos-
sible electrolyte abnormalities. In dogs, myocardial con-
tusion is the most common cardiac injury secondary to
thoracic trauma; premature ventricular contractions
and ventricular tachycardia are the most common ar-
rhythmias. The onset of arrhythmia may be delayed for
12 to 48 hours after trauma.2 Myocardial ischemia may

PREMEDICATION ■ ARRHYTHMIA ■ MYOCARDIAL CONTUSION

Small Animal/Exotics 20TH ANNIVERSARY
result from inadequate circulation or hypoxia and also
predisposes trauma patients to arrhythmias. Reperfu-
sion of ischemic myocardium may be associated with
transient reduced contractile efficiency.3 Severe blunt
chest trauma can produce multiple rib fractures, flail
segments, and pulmonary contusions, all of which pro-
duce pain and diminished pulmonary function.4
The primary concern and most common sequela of
head injury is increased intracranial pressure (ICP),
which may result from intracranial hemorrhage or cere-
bral edema. A hypoventilating trauma patient will exac-
erbate increased ICP because hypercapnia (increased
carbon dioxide) results in cerebral vasodilation and fur-
ther increases in cerebral blood flow.5
Because of the urgency of surgical intervention, fast-
ing trauma patients for the recommended 8 hours be-
fore general anesthesia is usually not possible. Trauma
slows gastric emptying, primarily due to shock and
pain-induced sympathetic stimulation.5 Gastric empty-
ing can be further slowed by administration of a nar-
cotic analgesic given to treat pain or sedate patients for
examination and treatment. To prevent aspiration, the
transition period between awake and anesthetized states
should be short. Intubation should be rapid and the en-
dotracheal tube cuff inflated while the patient is in ster-
nal recumbency with its head elevated.
PREMEDICATION
Anticholinergics
Anticholinergic drugs (e.g., atropine and glycopyrro-
late), which are often used as part of a preanesthetic
regimen, should be avoided in trauma patients unless
bradycardia exists. Although they reduce the volume
and acidity of gastric contents,6 anticholinergics in-
crease the incidence of arrhythmias (lower the thresh-
old for dysrhythmias) and anticholinergic-induced
tachycardia increases myocardial oxygen consumption.7
This may be detrimental in hypovolemic patients or
those with underlying myocardial contusions.
Tranquilizers
Benzodiazepines have amnesic, sedative, hypnotic,
anxiolytic, and anticonvulsant properties. Benzodi-
azepines alone do not provide adequate sedation in
healthy dogs and cats and may in fact produce paradox-
ic excitement.8 Thus, benzodiazepine tranquilizers may
be unreliable in alert trauma patients but may provide
desired mild sedation and muscle relaxation in those
with mild central nervous system (CNS) depression, es-
pecially when combined with such drugs as opioids.
Extreme CNS depression has been reported in already
depressed dogs, even at lower doses.8
Benzodiazepines exert their sedative effects by binding
INTRACRANIAL PRESSURE ■ BENZODIAZEPINES ■ ACEPROMAZINE
Compendium September 1999
to and activating the benzodiazepine receptor in the CNS
within the γ-aminobutyric acid (GABA)–receptor com-
plex. This results in opening of the chloride channels,
subsequently eliciting the CNS effects of benzodiazepines.
The GABA-receptor complex has other binding sites, per-
mitting the potentiation between benzodiazepines and
other agents.9 The skeletal muscle relaxation caused by
benzodiazepines is produced by their interaction with
glycine receptors at spinal levels. 10 Benzodiazepines
should not be used to treat pain because they do not pos-
sess clinically significant analgesic effects.11 If analgesia is
needed in addition to mild sedation, combination with
butorphanol, oxymorphone, fentanyl, or morphine in
small incremental doses often produces the desired result.
The benzodiazepines most commonly used in veteri-
nary medicine are diazepam and midazolam. Midazo-
lam is significantly (16 times) more expensive than is
diazepam but is two to four times more potent.12 Mida-
zolam causes less pain on injection, a greater degree of
early sedation, and a more rapid return to baseline
function.12,13 Midazolam is water soluble, providing bet-
ter intramuscular absorption with rapid onset (5 to 15
minutes). Diazepam is not recommended for intramus-
cular use because of its slow and erratic uptake.9
Benzodiazepines maintain cardiovascular stability8,12
but may induce respiratory depression, the severity of
which is dose-dependent.14 Significant cardiovascular
depression can occur if intravenous diazepam is admin-
istered rapidly. This depression is believed to be due to
the propylene glycol carrier, which is not present in mid-
azolam.15 In head trauma patients, diazepam has been
shown to effectively reduce cerebral metabolism and
decrease cerebral blood flow, thereby reducing ICP.16
Acepromazine is a phenothiazine tranquilizer possess-
ing marked sedative properties without analgesic activi-
ty. Acepromazine has potent α1-antagonist effects that
result in hypotension secondary to peripheral vasodila-
tion, which may be profound in animals with preexist-
ing hypovolemia and shock. This drug should therefore
be avoided in acute trauma patients. Other effects of
acepromazine include hypothermia, which is caused by
cutaneous vasodilation and increased heat loss as well as
alteration of the thermoregulatory mechanism, and a
moderate antiemetic effect, particularly against opioid-
induced vomiting.17
Acepromazine has little effect on respiration and may
in fact protect the heart from cardiac dysrhythmia.18
This antiarrhythmic effect is believed to be caused by a
blocking action on cardiac α-arrhythmic receptors.19
Because of its antiarrhythmic effects, acepromazine
may be useful later in the recovery process when hypo-
volemia and shock are resolved. For example, in combi-
nation with postoperative opioids, acepromazine may
Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE II nists should be avoided in all trauma pa-

Classes of Opiate Receptors and Their Effects tients because of an initial transient hy-
pertension, followed by prolonged hy-
Receptor Location Effect potension, as well as bradyarrhythmias,
µ Spinal (µ2) Respiratory depression, reduced including first- and second-degree atri-
Supraspinal (µ1) gastrointestinal motility, nausea, oventricular block.22 In addition, these ag-
emesis, pruritus onists sensitize the myocardium to cate-
cholamines.21 In trauma patients, all of
κ Spinal (κ1) Diuresis, sedation, miosis these effects may be serious. The extreme
Supraspinal (κ3) cardiovascular depression induced by
Unknown (κ2)
these drugs may unmask preexisting hy-
δ Spinal Modulation of µ-receptor activity potension or hypovolemia that is present
Supraspinal in most acutely traumatized patients.23
Even the newly available and easily re-
versible medetomidine will induce respi-
help to prevent ventricular arrhythmia secondary to ratory depression and bradycardia at standard dosages
pain, stress, and anxiety.18 If sedation is desired in pa- and should be used only in healthy patients.21,24
tients in which shock and severe blood loss are no
longer a concern (e.g., for postoperative or follow-up Opioids
radiography), acepromazine can be combined with bu- Three major classes and several subclasses of opiate re-
torphanol or oxymorphone for neuroleptanalgesia.20 ceptors are recognized and are present in the CNS, spinal
α2-Adrenoreceptor agonists (e.g., xylazine, medeto- cord, and peripheral tissue (Table II). The opiate recep-
midine) are used primarily for their profound sedation tors most often involved in supraspinal and spinal anal-
via stimulation of receptors centrally and provide excel- gesia as well as in narcotic side effects are the µ and κ re-
lent (but transient) analgesia via stimulation of recep- ceptors. Stimulation of the µ receptor produces analgesia
tors both centrally and peripherally.21 However, α2 ago- but also depresses respiration and gastrointestinal motili-

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Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

TABLE III dent, whereas the agonist–antagonists have a “ceiling

Classification of Opioid Drugs effect” (i.e., over a certain dose, additional drug does
not cause further respiratory depression).28 Low doses of
Drug µ Receptor κ Receptor opioid analgesics used for sedation or analgesia in trau-
Agonists ma patients may actually improve respiratory function
Morphine
Oxymorphone
Hydromorphone
{ Agonists Agonists
via effective pain control. In trauma patients with seri-
ous preexisting respiratory compromise that are about
to be intubated, opioids are a good choice for anesthe-
Fentanyl sia when, because of controlled ventilation, hypoventi-
Meperidine lation is no longer a concern.
In head trauma patients not requiring ventilation,
Partial Agonists opioids should be administered cautiously because hy-
Buprenorphine Partial agonist Unknown poventilation-induced increases in arterial carbon diox-
Codeine Agonist Agonist ide partial pressure will further increase ICP.16 When
analgesia is needed in patients with head trauma or hy-
Agonist–antagonists povolemia, low doses of opioids should be administered
Butorphanol Antagonist Agonist slowly while the patient is carefully monitored. When
Nalbuphine Antagonist Agonist complications occur, complete reversal of the respirato-
ry, cardiovascular, and analgesic effects may be achieved
Antagonists
using the opioid antagonist naloxone. When agonists
Naloxone Antagonist Antagonist
Naltrexone Antagonist Antagonist
have been administered, partial reversal is possible us-
Levallorphan Antagonist Antagonist ing either butorphanol or nalbuphine. This latter meth-
od is preferred in trauma patients because it maintains
some degree of analgesia while reversing most of the
ty and may even induce emesis. κ receptors are the pre- respiratory depression induced by agonist opioids.29
dominant opiate receptors in the brain9; the effect of
stimulating this receptor, in addition to analgesia, is se- INDUCTION
dation with less undesirable respiratory depression. The Barbiturates
δ receptor, present in the brain and spinal cord, is be- Barbiturates are not recommended in acutely trau-
lieved to play a smaller role in analgesia. matized patients with cardiovascular instability. These
The narcotic analgesics have variable affinity for the drugs are myocardial depressants that reduce cardiac
opiate receptors, and the sequelae of the receptor activa- output and stroke volume as well as peripheral vascular
tion depend on the opioid used and the specific receptor resistance.30 Thiobarbiturates sensitize the myocardium
activated (Table III). The most common agents are classi- to catecholamines, which can predispose patients to
fied as agonists (e.g., morphine, oxymorphone, hydromor- cardiac arrhythmias,31 and cause respiratory depression.
phone, fentanyl, meperidine), partial agonists (e.g., Although the cardiovascular and respiratory effects of
buprenorphine, codeine), or agonist–antagonists (e.g., bu- barbiturates are short-lived, they are poorly tolerated by
torphanol, nalbuphine). Pure antagonists (e.g., naloxone, trauma patients with cardiovascular instability.
nalorphine, levallorphan) are used for narcotic reversal. In head trauma patients with minimal cardiovascular
Overall heart rate, blood pressure, and systemic vascu- compromise, barbiturates are the preferred drug for in-
lar resistance remain relatively stable after opioid admin- duction of anesthesia because they decrease cerebral
istration.25,26 Intravenously administered meperidine and blood flow, cerebral metabolism, and ICP.16 However,
morphine are associated with hypotension, which is be- patients must be well ventilated because barbiturate-as-
lieved to result from dose-dependent, histamine-induced sociated respiratory depression leads to carbon dioxide
arteriolar and venous dilation.20 In contrast, oxymor- retention and an undesirable increase in cerebral blood
phone, hydromorphone, and fentanyl—also pure ago- flow and volume. When intubating patients, it is also
nists—are associated with less histamine release and thus important to prevent cough reflex to avoid an unwant-
more hemodynamic stability.9,20 Administering opioids ed sudden increase in ICP.
to patients with preexisting hypovolemia may further de-
crease mean arterial pressure. Propofol
The most significant adverse side effect of opioid ad- Propofol is a novel, ultrashort-acting, sedative–hyp-
ministration is respiratory depression.27 The respiratory notic agent that has been approved for use in dogs and
depression induced by agonist opioids is dose depen- cats. Propofol is lipid soluble and is formulated with a

OPIATE RECEPTORS ■ RESPIRATORY DEPRESSION ■ PARTIAL REVERSAL

Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

soybean oil–glycerol–egg emulsion carrier. This oil car-
rier and the lack of antimicrobial preservative allow for
the vehicle’s capability of supporting the growth of vari-
ous bacteria and Candida species.32 The drug has ex-
tremely rapid uptake and distribution and is very rapid-
ly eliminated, making it an ideal agent when a full and
rapid recovery is desirable.33 The highly protein-bound
propofol is conjugated in the liver by glucuronidation
to inactive glucuronide or sulfate metabolites, which
are subsequently excreted by the kidney.32
Propofol can be administered at low sedative doses to
control patient movement during radiographs or at
higher doses (to effect) to facilitate endotracheal intu-
bation for general anesthesia or ventilation. Because
propofol lacks cumulative effects, additional incremen-
tal intravenous doses can be administered safely to pro-
long anesthesia duration without significantly affecting
anesthesia recovery time.
Like barbiturates, propofol causes a reduction in
cerebral blood flow and ICP that may be beneficial in
head trauma patients.16 However, there are significant
potential adverse effects associated with propofol.
Propofol can cause apnea, particularly on induction,
and is a potent respiratory depressant. Cyanosis and res-
piratory arrest will occur with rapid administration.32 A
reduction in systemic vascular resistance due to vasodi-
lation as well as a dose-related decrease in myocardial
contractility have been observed with propofol admin-
istration.34 As a result, like barbiturates, this drug is not
recommended for use in trauma patients with cardio-
vascular compromise, especially hypovolemia or hy-
potension.35
Propofol has no analgesic properties; supplementa-
tion with an analgesic agent therefore must be consid-
ered, especially when propofol is used to maintain anes-
thesia during painful procedures. In these cases, pre- or
intraoperative administration of an opiate (e.g., oxy-
morphone or butorphanol) is recommended.
Etomidate
Etomidatea is a very safe, ultrashort-acting hypnotic
anesthetic with a rapid onset of action and poor anal-
gesic properties. The cardiovascular system is minimally
affected by etomidate,36 even in the presence of hypo-
volemia,37 making it ideal for use in hemodynamically
unstable trauma patients or those with preexisting car-
diac disease. In addition, respiratory depression is not
associated with this drug.36
Etomidate can cause pain on injection, and retching,
emesis (sometimes violent), sneezing, and defecation
aFor
more information on etomidate, see the Pharm Profile col-
umn in the June 1999 (Vol. 21, No. 6) issue of Compendium.

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Nautrup and Tobias
■ Sonographic diagnosis in dogs and cats, including
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Small Animal/Exotics
are common during induction.38 Etomidate also results
in marked adrenal suppression (2 to 6 hours), inhibit-
ing the normal increase in plasma cortisol and aldos-
terone that occurs during stress.39
Etomidate is excellent as an intravenous induction
agent for general anesthesia, for short procedures (5 to
10 minutes), and to maintain sedation in critical pa-
tients. Premedication (e.g., with diazepam or an opi-
oid) is necessary to avoid undesirable side effects during
induction and to provide sufficient analgesia, particu-
larly when painful manipulations are being performed
in trauma patients. Despite the many advantages of this
drug, however, its cost and availability may prohibit its
use in many clinical situations.
Opioids
Opioids and benzodiazepines administered together
cause minimal cardiovascular depression and make an
excellent induction combination in hypovolemic or de-
hydrated patients. In trauma patients with cardiac ar-
rhythmias or depression, opioids are useful for anesthe-
sia induction if they are used in combination with a
tranquilizer for neuroleptanalgesia.
Unlike rapid induction techniques, patients are often
still arousable after drug administration and intubation
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20TH ANNIVERSARY Compendium September 1999
is possible by gently opening the mouth and carefully
avoiding activation of the gag reflex. Naloxone, a pure
opioid antagonist, is often used to reverse the effects of
sedation for quicker recovery in critical patients.
Ketamine
Ketamine combined with diazepam is an excellent
induction agent for patients with mild to moderate
shock. Although ketamine has a direct myocardial de-
pressant action, its indirect effects, mediated via sympa-
thetic stimulation, cause an increase in cardiac output,
heart rate, and blood pressure.8 In normovolemic ani-
mals and humans, ketamine alone produces hyperten-
sion and tachycardia.40 These effects are attenuated
when coupled with a tranquilizer, such as diazepam, xy-
lazine, or acepromazine.
Ketamine has been advocated for use in hypovolemic
patients because it supports the poorly compensated
cardiovascular system.41 If combined with diazepam,
ketamine provides muscle relaxation without interfer-
ing with the sympathetic stimulation it induces. In
severely hypovolemic patients with maximal sympathet-
ic output, ketamine may not have an advantage over
such drugs as thiopental.42 Ketamine cannot mobilize a
patient’s already exhausted catecholamines and there-
fore can be as depressing to the cardiovascular system as
is thiopental.
Ketamine also markedly increases cerebral blood flow,
• Easy Reference Index with a concomitant increase in ICP.16 Although com-
• 364 Pages bining ketamine with diazepam attenuates this re-
• Color and sponse, it does not protect head injury patients from
Black-and-White
Photographs further elevations in ICP. Therefore, ketamine alone or
in combination with diazepam is not recommended for
use in head trauma patients.
Medicine
Neuromuscular Blocking Agents
There are two major types of muscle relaxants—de-
polarizing and nondepolarizing agents. Depolarizing
muscle relaxants (e.g., succinylcholine) act by binding
to acetylcholine-receptor sites and depolarizing the
quent action potentials. Muscle relaxation is very rapid,
tice
COLLE
The
COMPENDIUM
CTION
but the effect is very short. Nondepolarizing muscle re-
laxants (e.g., atracurium, vecuronium, pancuronium)
act by competing with acetylcholine for binding at the
nerve endplate and preventing depolarization of the
nerve. These agents vary in duration of action from
short to long acting. Neuromuscular blocking drugs do
not provide loss of consciousness or analgesia and
should not be used for painful procedures (e.g., fracture
VLS BOOKS stabilization) without supplemental analgesics or gener-
VE T E R I N A RY L E A R N I N G SYS T E M S
al anesthetics.
Because the onset of action of succinylcholine is very
NALOXONE ■ HYPOVOLEMIA
 Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

rapid (30 to 60 seconds) and the duration of action is
brief (3 to 7 minutes), it is often used for emergency
rapid intubation. However, succinylcholine has signifi-
cant undesirable side effects. It may result in various
bradyarrhythmias or tachyarrhythmias; muscle fascicu-
lations; increases in serum potassium; and increases in
intraocular, intracranial, and intragastric pressure.43
Therefore, the use of succinylcholine is contraindicated
in patients with cardiac arrhythmias, suspected hyper-
kalemia, ocular injuries, or head trauma. If succinyl-
choline is administered with halothane, severe hyper-
thermia may develop.44
Nondepolarizing agents have some advantages over
depolarizing agents. In general, nondepolarizing agents
provide smoother relaxation and a longer duration of
action and the paralysis can be partially reversed by an-
ticholinesterase drugs (e.g., neostigmine, pyridostig-
mine, edrophonium). Atra-
END IU curium is short acting (25
MP
to 35 minutes) and is associ-
M’
sia. All volatile agents increase cerebral blood flow,
thereby potentially increasing ICP. Low doses of isoflu-
rane have little effect on cerebral pressures if the patient
is hyperventilated. Isoflurane and halothane have negli-
gible analgesic properties.
Isoflurane is the safest inhalant anesthetic in animals
with traumatic myocarditis or preexisting cardiac dis-
ease.47 Isoflurane causes less cardiac depression than
does halothane, and induction and recovery are rapid.
However, isoflurane can cause significant hypotension
secondary to peripheral vasodilation. Halothane is a
myocardial depressant and can predispose patients to
cardiac arrhythmias as it sensitizes the heart to cate-
cholamines.48 This is particularly important in trauma
patients, and even more so if acidosis or hypoxia is also
present. Isoflurane does not sensitize the myocardium
to catecholamines and therefore tends not to be ar-
rhythmogenic.49
Nitrous oxide can reduce the amount of halothane or
isoflurane required or can be used as a 50/50 nitrous

20th

CO

S

1 9 7
9 - 1
9 9 9ated with histamine release oxide/oxygen mixture in sedated patients. Nitrous ox-
ANNIVERSARY and subsequent hypoten- ide alone is not capable of producing general anesthesia
sion. Histamine release can adequate for surgery but does provide some analgesia in
A LookBack be minimized with slow in-
jection of the drug whereby
addition to muscle relaxation. Nitrous oxide can diffuse
into the pleural space and is contraindicated in the
Trauma patients are generally the time to onset of paraly- presence of a possible pneumothorax. A minimum of
an extremely high-risk
sis is progressive over 2 to 5 30% oxygen should always be administered when ni-
minutes.45 Vecuronium is an trous oxide is used.50 When nitrous oxide is adminis-
population. Over the past few
intermediate-acting (35 to tered in concentrations of 50% or greater, the amount
decades, the use of isoflurane—
45 minutes) neuromuscular of oxygen delivered to the patient is reduced. This is
a newer, safer volatile agent— blocker that is not associat- critical in trauma patients if oxygenation is impaired
has increased in practices. Use ed with histamine release and (e.g., pulmonary contusions or anemia due to hemor-
of isoflurane and halothane has has no adverse effects on the rhage).51 Nitrous oxide does have the potential to seri-
replaced the previously common cardiovascular system.46 Pan- ously depress the contused myocardium.
use of methoxyflurane. New curonium is a long-acting
injectable anesthetics have (70 to 90 minutes) neuro- CONCLUSION
emerged that are rapidly muscular blocker with a An anesthetic agent is not a substitute for adequate
metabolized and have a much slow onset of action; al- restoration of blood volume and venous return. When
greater margin of safety than though it does not produce an anesthetic agent must be administered to a patient
that of some agents used
histamine release, it can be with significant hypovolemia, cardiovascular depression
associated with tachycardia should be expected. Hypovolemia will reduce the over-
routinely previously. Some of
and increased blood pres- all anesthetic requirements in the patient.
these new agents, including
sure via a vagolytic effect.46 Sedative agents used in trauma patients should have a
opioids, are potentially rapid elimination time to avoid prolonged undesired
reversible. However, despite MAINTENANCE: sedation. Rapid reversibility of sedation allows for peri-
wide acceptance and increasing INHALATION odic patient assessment. Sedative agents must be not
use of these newer, safer agents, ANESTHETICS only rapidly reversible but also effective to achieve the
the use and benefits (including All inhalation anesthetics desired outcome.
cost) of the older agents (e.g., induce at least some degree The sedative or anesthetic regimen used in trauma
thiobarbiturates) remain among of dose-dependent respirato- patients must provide analgesia. Pain is a major factor
the general veterinary ry and cardiovascular de- associated with the hemodynamic and respiratory insta-
patient population. pression, which increases bility observed in trauma patients, and pain control has
with the depth of anesthe- been shown to improve pulmonary function.52

NONDEPOLARIZING AGENTS ■ ISOFLURANE ■ HALOTHANE

Small Animal/Exotics 20TH ANNIVERSARY
Special monitoring equipment useful for trauma pa-
tients includes arterial and central venous pressure
catheters, urinary catheters for urine output, esophageal
stethoscopes, electrocardiographic monitors, pulse oxim-
eters, capnometers, and indirect blood pressure devices.
Placing an arterial line is useful when multiple samples
for packed cell volume or electrolytes or multiple arteri-
al blood gas determinations must be obtained.
If we assume the worst can happen during anesthesia,
then we are likely to watch for complications and inter-
vene in an appropriate and timely manner. Close pa-
tient monitoring often continues beyond surgery and
recovery in trauma patients. The more critical or unsta-
ble the patient is, the greater is the number of monitor-
ing devices employed.
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About the Authors
Dr. Garrod is affiliated with New England Veterinary Spe-
cialists in Brentwood, New Hampshire. Dr. Wetmore is af-
filiated with the Department of Clinical Sciences, School
of Veterinary Medicine, Tufts University, North Grafton,
Massachusetts, and is a Diplomate of the American Col-
lege of Veterinary Anesthesiologists.