Anesthetic Agents In Trauma Patients

V CE

20TH ANNIVERSARY

Vol. 21, No. 9 September 1999

Refereed Peer Review

FOCAL POINT

Anesthetic Agents in Trauma Patients

★ 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.

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 discusses the mechanisms of action, advantages, and disadvantages of certain anesthetic agents, including anticholinergics, α2 adrenoreceptor agonists, phenothiazines, benzodiazepines, opioids, barbiturates, propofol, etomidate, ketamine, neuromuscular blockers, and volatile anesthetics.

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 injuries must be identified and treated based on the potential risk of mortality that they pose to the patient. Maintenance of a patent airway and intravascular volume resuscitation are primary considerations. Patients that present with major, multiple traumatic injuries may require sedation, chemical restraint, or general anesthesia so that life-saving diagnostic and therapeutic procedures can be performed. Such patients pose a tremendous challenge 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 anesthetic agent that provides analgesia and relaxation without depressing respiration or compromising cardiovascular stability. Every effort should be made to stabilize trauma patients before the induction of anesthesia. Only in unusual circumstances, such as continuing massive hemorrhage or closed head trauma with intracranial hemorrhage, is it inadvisable to completely correct hypovolemia and shock before surgical intervention. Trauma patients are likely to have decreased anesthetic requirements and unpredictable 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

Diazepam Midazolam

0.2 IV 0.2 IM or IV

Hemodynamic stability; reduce intracranial pressure

Propylene glycol carrier in diazepam may cause hypotension and bradycardia with rapid IV administration

0.5–1 IM or IV 1–2 IM (cats) 0.05–0.2 IM or IV 0.05–0.2 IM or IV 0.01–0.04 IM or IV 0.2–0.4 SC, IM, or IV 0.01 IM or IV

Cardiovascular stability; no effect on intracranial pressure; analgesia (varying potency); reversed with antagonist

Dose-dependent respiratory depression and bradycardia

Thiopental

10 IV

Decreases intracranial pressure

Myocardial depression; arrhythmias; respiratory depression

Ketamine

2–5 IV with diazepam

Minimal cardiovascular depression

Increases intracranial pressure

Propofol

4–8 slow IV 0.2–0.3 mg/kg/min CRI

Ultrashort-acting; reduces intracranial pressure

Profound respiratory depression or apnea; hypotension; aseptic handling; no analgesia

Very safe; ultrashort-acting; cardiovascular stability; no respiratory depression

Very expensive; poor analgesia; emesis and defecation on induction and recovery unless proper premedication

All but succinylcholine can be partially reversed; little to no adverse side effects

Patient must be intubated and ventilated; increased intraocular pressure with succinylcholine

Isoflurane causes less cardiac depression than does halothane; rapid induction and recovery with isoflurane

Respiratory and myocardial depression; potential increase in intracranial pressure; halothane arrhythmogenic as it sensitizes the myocardium to catecholamines

Morphine Meperidine Oxymorphone Hydromorphone Fentanyl Butorphanol Buprenorphine

Etomidate

Succinylcholine Pancuronium Atracurium Vecuronium Halothane Isoflurane

0.5–1 IV

0.3–0.4 IV 0.02–0.06 IV 0.2–0.4 IV 0.1 IV To effect (1.5 MAC)

Disadvantages

CRI = constant-rate infusion; IM = intramuscular; IV = intravenously; MAC = minimum alveolar concentration; SC = subcutaneously.

is already dehydrated and hypovolemic, can cause severe hypotension.1 As a result, the initial dose of any anesthetic agent used should be halved and subsequently titrated to effect. Premedication may not be necessary in some patients. Agents administered subcutaneously 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, endogenous catecholamine release, hypothermia, and possible electrolyte abnormalities. In dogs, myocardial contusion is the most common cardiac injury secondary to thoracic trauma; premature ventricular contractions and ventricular tachycardia are the most common arrhythmias. The onset of arrhythmia may be delayed for 12 to 48 hours after trauma.2 Myocardial ischemia may

PREMEDICATION ■ ARRHYTHMIA ■ MYOCARDIAL CONTUSION

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20TH ANNIVERSARY

result from inadequate circulation or hypoxia and also predisposes trauma patients to arrhythmias. Reperfusion 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 produce 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 cerebral edema. A hypoventilating trauma patient will exacerbate increased ICP because hypercapnia (increased carbon dioxide) results in cerebral vasodilation and further increases in cerebral blood flow.5 Because of the urgency of surgical intervention, fasting trauma patients for the recommended 8 hours before general anesthesia is usually not possible. Trauma slows gastric emptying, primarily due to shock and pain-induced sympathetic stimulation.5 Gastric emptying can be further slowed by administration of a narcotic 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 endotracheal tube cuff inflated while the patient is in sternal recumbency with its head elevated.

PREMEDICATION Anticholinergics Anticholinergic drugs (e.g., atropine and glycopyrrolate), 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 increase the incidence of arrhythmias (lower the threshold 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. Benzodiazepines alone do not provide adequate sedation in healthy dogs and cats and may in fact produce paradoxic 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, especially 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

Compendium September 1999

to and activating the benzodiazepine receptor in the CNS within the γ-aminobutyric acid (GABA)–receptor complex. This results in opening of the chloride channels, subsequently eliciting the CNS effects of benzodiazepines. The GABA-receptor complex has other binding sites, permitting 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 possess 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 veterinary medicine are diazepam and midazolam. Midazolam is significantly (16 times) more expensive than is diazepam but is two to four times more potent.12 Midazolam 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 better intramuscular absorption with rapid onset (5 to 15 minutes). Diazepam is not recommended for intramuscular 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 administered rapidly. This depression is believed to be due to the propylene glycol carrier, which is not present in midazolam.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 possessing marked sedative properties without analgesic activity. Acepromazine has potent α1-antagonist effects that result in hypotension secondary to peripheral vasodilation, which may be profound in animals with preexisting 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 opioidinduced 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 hypovolemia and shock are resolved. For example, in combination with postoperative opioids, acepromazine may

INTRACRANIAL PRESSURE ■ BENZODIAZEPINES ■ ACEPROMAZINE

Compendium September 1999

20TH ANNIVERSARY

Small Animal/Exotics

nists should be avoided in all trauma patients because of an initial transient hypertension, followed by prolonged hyReceptor Location Effect potension, as well as bradyarrhythmias, including first- and second-degree atriµ Spinal (µ2) Respiratory depression, reduced Supraspinal (µ1) gastrointestinal motility, nausea, oventricular block.22 In addition, these agemesis, pruritus onists sensitize the myocardium to catecholamines.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 hypotension or hypovolemia that is present δ Spinal Modulation of µ-receptor activity in most acutely traumatized patients.23 Supraspinal Even the newly available and easily reversible medetomidine will induce respihelp to prevent ventricular arrhythmia secondary to ratory depression and bradycardia at standard dosages pain, stress, and anxiety.18 If sedation is desired in paand should be used only in healthy patients.21,24 tients in which shock and severe blood loss are no Opioids longer a concern (e.g., for postoperative or follow-up Three major classes and several subclasses of opiate reradiography), acepromazine can be combined with buceptors are recognized and are present in the CNS, spinal torphanol or oxymorphone for neuroleptanalgesia.20 α2-Adrenoreceptor agonists (e.g., xylazine, medetocord, and peripheral tissue (Table II). The opiate recepmidine) are used primarily for their profound sedation tors most often involved in supraspinal and spinal analvia stimulation of receptors centrally and provide excelgesia as well as in narcotic side effects are the µ and κ receptors. Stimulation of the µ receptor produces analgesia lent (but transient) analgesia via stimulation of recepbut also depresses respiration and gastrointestinal motilitors both centrally and peripherally.21 However, α2 agoTABLE II Classes of Opiate Receptors and Their Effects

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Patrici -IN-CHIE F: a M. DACV Dowling, IM, DA DV CVCP M, MS,

EDITORI

Volum e 1,

Num AL R Mark EVIEW ber 1 Ander BOA • Win son, DACV DVM, RD: ter 20 S MS, Joseph 00 W. Bar tges, DACV DVM, IM, John PhD, Bauer, DACVN Byron DV Blagbu M, PhD Frank rn, PhD , DACV Blecha N Dawn , Merto BS, MS, PhD n Boo MS, the PhD, DACV , DVM, DACV IM, Wendy CP C. Bro wn, PhD BA, MP Dennis H, Chery J. Chew, l Chrism DVM, an, DV DACVIM DACV IM M, MS Noah , Cohen, Linda DeBow VMD, PhD es, DV DACV M, MS IM, John , Deen, DAVDC DVM, DABV MSc, P Susan PhD, Donog hue, DACV VMD, N Gregg MS, DuPon Dunca t, DV n Fer M, DA DACV guson, VM VDC IM, DA D, PhD Richar CVCP , d B. Ford, Lisa Fre DV Robert eman, DV M, MS M, PhD Friends Frankl in Gar hip, DVM, ry, DV MSc DACV M, MS IM Larry , Glickm an, VM MA, D, MP Effect Deena DrPH H, of Gregor Peter and Gi Clindamyci y, DV J. Ihr M ng DACV ke, VMD, J.M. Wa ivitis in Do n Hydroch DACV D Lesley loride rrick, IM, G. Kin on G.A. Ins gs with Pe g, MV DACV B, MR keep, T.D riodonti Oral Malo IM, DA CVS, Satiety DECV dor, Pla CVEC . Yonker tis IM C, Fred Re que, Ca s, G.K. Lehma D.E. Jew duces Ad lculus n, DV Stooke ipo DACT ell, P.W M, MA , y, and Michae BM, . Toll, sity in Dogs T.H. Ew and B.J Clinto l S. Leib, ing Effect DVM, . n D. No votny s Lothro MS PhD p, Jr., Bioch of a 1% Hy Sandy , DACVIM DVM, emica dro Love, corti l Param React BVMS CVS ivi , PhD eters, sone Cond Steve , MR Adren R.C. Th ty to Hista itione Marks al r on mi , BVSc, omas, DACV D. Lo ne in Norm Function Te Hematol MS, IM Karol MRCV gas, L. ogic an Ann S, Rados al and Pru sting, and Mathe Effica d PhD ta, an ws, DV cy Glenn , DACVEC d J. Ha ritic Dogs Cutaneous M, in Ro of Two Ca a C rrison ttw Sheila Mauldin, nine Pa DV McGu Materna eiler and rvovir Kathry irk, DV M Do us n E. M.J. Co lly Derived berman Pin Vaccines Michel M, PhD Paul S. , for Ind yne Antib sch Gene Morley, DV DVM, MS er odies uc Pups H. Nes M, PhD with Va ing Seroc bitt, DACV DVM, on Evalu rio D ver Mary MS, us Level sion ati Ann Nie s of Mark Used on in Vitro Papich ves, DVM, in the Barbar , DV Manage of the Antim D.H. M, MS MS a Lloyd Rebecc Powers, c icrob DVM, and A.I ment of a L. Rem Ear Inf ial Activity . Lamp MS, illard, MS ection DVM, ort James PhD Respo s in the of Two Topic A. Rot nse h, DV DACV Dog al Pre Regular to Modifie M, MS paration Michae M , PhD ly d Va Liv , l Sch s E.J. Du cci e aer, DV DACV bovi, Y.T nated, Fre and Killed M, 43 Sue Sem IM, DA sh Da . Gröhn CVEC rad, iry Co Multivalent C Mary , M.A. DVM Viral Anna Salmon Brunn ws Willia Thrall, Vaccine ella der er, and m Tra K.J. Gr in nquilli DVM, MS J.A. He DACV oninga by Cross-Pr , DV A rtl M, MS Victor , E. Spr otecti ia L. , on inger, 49 DACV Voith, DV M. Bra Study Instru M, PhD Dennis B un cti schmidt, , ons to Bryan P. Wages Autho and D. , DV M. Wa rs Pankrat ldridg M, DACP Call for DABV V e, DV P z Stephe M, MS Papers n D. , DACV White, DV 59 D From M,

Inaugu ral Iss ue

Vete Thera rinary peuti cs

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Resea rch in Appli ed Vet erina ry Med icine

Table of Co nten ts

the Ed itors Mission Statem ent

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Small Animal/Exotics

20TH ANNIVERSARY

TABLE III Classification of Opioid Drugs µ Receptor

κ Receptor

Agonists

Agonists

Partial agonist Agonist

Unknown Agonist

Agonist–antagonists Butorphanol Nalbuphine

Antagonist Antagonist

Agonist Agonist

Antagonists Naloxone Naltrexone Levallorphan

Antagonist Antagonist Antagonist

Antagonist Antagonist Antagonist

Drug Agonists Morphine Oxymorphone Hydromorphone Fentanyl Meperidine

{

Partial Agonists Buprenorphine Codeine

ty and may even induce emesis. κ receptors are the predominant opiate receptors in the brain9; the effect of stimulating this receptor, in addition to analgesia, is sedation with less undesirable respiratory depression. The δ receptor, present in the brain and spinal cord, is believed to play a smaller role in analgesia. The narcotic analgesics have variable affinity for the opiate receptors, and the sequelae of the receptor activation depend on the opioid used and the specific receptor activated (Table III). The most common agents are classified as agonists (e.g., morphine, oxymorphone, hydromorphone, fentanyl, meperidine), partial agonists (e.g., buprenorphine, codeine), or agonist–antagonists (e.g., butorphanol, nalbuphine). Pure antagonists (e.g., naloxone, nalorphine, levallorphan) are used for narcotic reversal. Overall heart rate, blood pressure, and systemic vascular resistance remain relatively stable after opioid administration.25,26 Intravenously administered meperidine and morphine are associated with hypotension, which is believed to result from dose-dependent, histamine-induced arteriolar and venous dilation.20 In contrast, oxymorphone, hydromorphone, and fentanyl—also pure agonists—are associated with less histamine release and thus more hemodynamic stability.9,20 Administering opioids to patients with preexisting hypovolemia may further decrease mean arterial pressure. The most significant adverse side effect of opioid administration is respiratory depression.27 The respiratory depression induced by agonist opioids is dose depen-

Compendium September 1999

dent, whereas the agonist–antagonists have a “ceiling effect” (i.e., over a certain dose, additional drug does not cause further respiratory depression).28 Low doses of opioid analgesics used for sedation or analgesia in trauma patients may actually improve respiratory function via effective pain control. In trauma patients with serious preexisting respiratory compromise that are about to be intubated, opioids are a good choice for anesthesia when, because of controlled ventilation, hypoventilation is no longer a concern. In head trauma patients not requiring ventilation, opioids should be administered cautiously because hypoventilation-induced increases in arterial carbon dioxide partial pressure will further increase ICP.16 When analgesia is needed in patients with head trauma or hypovolemia, low doses of opioids should be administered slowly while the patient is carefully monitored. When complications occur, complete reversal of the respiratory, cardiovascular, and analgesic effects may be achieved using the opioid antagonist naloxone. When agonists have been administered, partial reversal is possible using either butorphanol or nalbuphine. This latter method is preferred in trauma patients because it maintains some degree of analgesia while reversing most of the respiratory depression induced by agonist opioids.29

INDUCTION Barbiturates Barbiturates are not recommended in acutely traumatized patients with cardiovascular instability. These drugs are myocardial depressants that reduce cardiac output and stroke volume as well as peripheral vascular resistance.30 Thiobarbiturates sensitize the myocardium to catecholamines, which can predispose patients to cardiac arrhythmias,31 and cause respiratory depression. Although the cardiovascular and respiratory effects of barbiturates are short-lived, they are poorly tolerated by trauma patients with cardiovascular instability. In head trauma patients with minimal cardiovascular compromise, barbiturates are the preferred drug for induction of anesthesia because they decrease cerebral blood flow, cerebral metabolism, and ICP.16 However, patients must be well ventilated because barbiturate-associated respiratory depression leads to carbon dioxide retention and an undesirable increase in cerebral blood flow and volume. When intubating patients, it is also important to prevent cough reflex to avoid an unwanted sudden increase in ICP. Propofol Propofol is a novel, ultrashort-acting, sedative–hypnotic agent that has been approved for use in dogs and cats. Propofol is lipid soluble and is formulated with a

OPIATE RECEPTORS ■ RESPIRATORY DEPRESSION ■ PARTIAL REVERSAL

Compendium September 1999

20TH ANNIVERSARY

soybean oil–glycerol–egg emulsion carrier. This oil carrier and the lack of antimicrobial preservative allow for the vehicle’s capability of supporting the growth of various bacteria and Candida species.32 The drug has extremely rapid uptake and distribution and is very rapidly 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 intubation for general anesthesia or ventilation. Because propofol lacks cumulative effects, additional incremental intravenous doses can be administered safely to prolong 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 respiratory arrest will occur with rapid administration.32 A reduction in systemic vascular resistance due to vasodi-

Small Animal/Exotics

lation as well as a dose-related decrease in myocardial contractility have been observed with propofol administration.34 As a result, like barbiturates, this drug is not recommended for use in trauma patients with cardiovascular compromise, especially hypovolemia or hypotension.35 Propofol has no analgesic properties; supplementation with an analgesic agent therefore must be considered, especially when propofol is used to maintain anesthesia during painful procedures. In these cases, pre- or intraoperative administration of an opiate (e.g., oxymorphone or butorphanol) is recommended.

Etomidate Etomidatea is a very safe, ultrashort-acting hypnotic anesthetic with a rapid onset of action and poor analgesic properties. The cardiovascular system is minimally affected by etomidate,36 even in the presence of hypovolemia,37 making it ideal for use in hemodynamically unstable trauma patients or those with preexisting cardiac 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 column in the June 1999 (Vol. 21, No. 6) issue of Compendium.

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are common during induction.38 Etomidate also results in marked adrenal suppression (2 to 6 hours), inhibiting the normal increase in plasma cortisol and aldosterone 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 patients. Premedication (e.g., with diazepam or an opioid) is necessary to avoid undesirable side effects during induction and to provide sufficient analgesia, particularly 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 dehydrated patients. In trauma patients with cardiac arrhythmias or depression, opioids are useful for anesthesia 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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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 depressant action, its indirect effects, mediated via sympathetic stimulation, cause an increase in cardiac output, heart rate, and blood pressure.8 In normovolemic animals and humans, ketamine alone produces hypertension and tachycardia.40 These effects are attenuated when coupled with a tranquilizer, such as diazepam, xylazine, 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 interfering with the sympathetic stimulation it induces. In severely hypovolemic patients with maximal sympathetic output, ketamine may not have an advantage over such drugs as thiopental.42 Ketamine cannot mobilize a patient’s already exhausted catecholamines and therefore can be as depressing to the cardiovascular system as is thiopental. Ketamine also markedly increases cerebral blood flow, with a concomitant increase in ICP.16 Although combining ketamine with diazepam attenuates this response, it does not protect head injury patients from further elevations in ICP. Therefore, ketamine alone or in combination with diazepam is not recommended for use in head trauma patients. Neuromuscular Blocking Agents There are two major types of muscle relaxants—depolarizing and nondepolarizing agents. Depolarizing muscle relaxants (e.g., succinylcholine) act by binding to acetylcholine-receptor sites and depolarizing the postjunctional membrane, thereby preventing subsequent action potentials. Muscle relaxation is very rapid, but the effect is very short. Nondepolarizing muscle relaxants (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 stabilization) without supplemental analgesics or general anesthetics. Because the onset of action of succinylcholine is very NALOXONE ■ HYPOVOLEMIA

Compendium September 1999

20TH ANNIVERSARY

S
M’

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 significant undesirable side effects. It may result in various bradyarrhythmias or tachyarrhythmias; muscle fasciculations; 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 hyperkalemia, ocular injuries, or head trauma. If succinylcholine is administered with halothane, severe hyperthermia 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 anticholinesterase drugs (e.g., neostigmine, pyridostigmine, edrophonium). Atracurium is short acting (25 D N E I U MP to 35 minutes) and is associated with histamine release ANNIVERSARY and subsequent hypotension. Histamine release can be minimized with slow injection of the drug whereby the time to onset of paralyTrauma patients are generally sis is progressive over 2 to 5 an extremely high-risk minutes.45 Vecuronium is an population. Over the past few intermediate-acting (35 to decades, the use of isoflurane— 45 minutes) neuromuscular a newer, safer volatile agent— blocker that is not associathas increased in practices. Use ed with histamine release and of isoflurane and halothane has has no adverse effects on the replaced the previously common cardiovascular system.46 Pancuronium is a long-acting use of methoxyflurane. New (70 to 90 minutes) neuroinjectable anesthetics have muscular blocker with a emerged that are rapidly slow onset of action; almetabolized and have a much though it does not produce greater margin of safety than histamine release, it can be that of some agents used associated with tachycardia routinely previously. Some of and increased blood presthese new agents, including sure via a vagolytic effect.46
CO

20th 9 9 9 9 - 1 1 9 7

A LookBack

opioids, are potentially reversible. However, despite wide acceptance and increasing use of these newer, safer agents, the use and benefits (including cost) of the older agents (e.g., thiobarbiturates) remain among the general veterinary patient population.

MAINTENANCE: INHALATION ANESTHETICS All inhalation anesthetics induce at least some degree of dose-dependent respiratory and cardiovascular depression, which increases with the depth of anesthe-

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sia. All volatile agents increase cerebral blood flow, thereby potentially increasing ICP. Low doses of isoflurane have little effect on cerebral pressures if the patient is hyperventilated. Isoflurane and halothane have negligible analgesic properties. Isoflurane is the safest inhalant anesthetic in animals with traumatic myocarditis or preexisting cardiac disease.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 catecholamines.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 arrhythmogenic.49 Nitrous oxide can reduce the amount of halothane or isoflurane required or can be used as a 50/50 nitrous oxide/oxygen mixture in sedated patients. Nitrous oxide alone is not capable of producing general anesthesia adequate for surgery but does provide some analgesia in addition to muscle relaxation. Nitrous oxide can diffuse into the pleural space and is contraindicated in the presence of a possible pneumothorax. A minimum of 30% oxygen should always be administered when nitrous oxide is used.50 When nitrous oxide is administered in concentrations of 50% or greater, the amount of oxygen delivered to the patient is reduced. This is critical in trauma patients if oxygenation is impaired (e.g., pulmonary contusions or anemia due to hemorrhage).51 Nitrous oxide does have the potential to seriously depress the contused myocardium.

CONCLUSION An anesthetic agent is not a substitute for adequate restoration of blood volume and venous return. When an anesthetic agent must be administered to a patient with significant hypovolemia, cardiovascular depression should be expected. Hypovolemia will reduce the overall anesthetic requirements in the patient. Sedative agents used in trauma patients should have a rapid elimination time to avoid prolonged undesired sedation. Rapid reversibility of sedation allows for periodic patient assessment. Sedative agents must be not only rapidly reversible but also effective to achieve the desired outcome. The sedative or anesthetic regimen used in trauma patients must provide analgesia. Pain is a major factor associated with the hemodynamic and respiratory instability observed in trauma patients, and pain control has been shown to improve pulmonary function.52

NONDEPOLARIZING AGENTS ■ ISOFLURANE ■ HALOTHANE

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Special monitoring equipment useful for trauma patients includes arterial and central venous pressure catheters, urinary catheters for urine output, esophageal stethoscopes, electrocardiographic monitors, pulse oximeters, capnometers, and indirect blood pressure devices. Placing an arterial line is useful when multiple samples for packed cell volume or electrolytes or multiple arterial blood gas determinations must be obtained. If we assume the worst can happen during anesthesia, then we are likely to watch for complications and intervene in an appropriate and timely manner. Close patient monitoring often continues beyond surgery and recovery in trauma patients. The more critical or unstable the patient is, the greater is the number of monitoring devices employed.

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About the Authors Dr. Garrod is affiliated with New England Veterinary Specialists in Brentwood, New Hampshire. Dr. Wetmore is affiliated with the Department of Clinical Sciences, School of Veterinary Medicine, Tufts University, North Grafton, Massachusetts, and is a Diplomate of the American College of Veterinary Anesthesiologists.