Myths and Misconceptions Wagner 2003

1426 Vet Med Today: Reference Point JAVMA, Vol 223, No. 10, November 15, 2003

Reference Point

The perianesthetic mortality rate for dogs and catshas been reported to range from 0.1% to 0.43%, butprobably varies greatly from 1 veterinary practice tothe next,1-4 with many veterinarians reporting a lowincidence of anesthesia-related deaths in their prac-tices. Nevertheless, even a rare anesthesia-related deathhas a marked impact on clients and the veterinary staff.Veterinary anesthesia has progressed to the point thatsurvival is no longer the only criterion for good or suc-cessful anesthesia. Modern anesthetic techniques aredesigned to minimize risks, not only of obvious com-plications but also of hidden ones, and to maximize theodds of a favorable outcome. In discussing anestheticdrug protocols and monitoring techniques with smallanimal veterinarians, the authors have become awareof certain myths or misconceptions shared by manypractitioners. In a medical community, beliefs oftenarise from a combination of clinical experience and theprevailing scientific evidence. As further research isconducted, many things that were once considered factare disproved, yet reevaluation of beliefs does notalways keep pace with the rate of scientific discovery.Thus, beliefs that were once evidence-based becomeoutmoded and fall into the realm of myth or miscon-ception.

The following comments are intended to refutesome of the myths and clarify certain misconceptionssurrounding the practice of small animal anesthesia,present current understanding of commonly misun-derstood issues, and aid practitioners in providinghigher quality care for their small animal patients.

Myth—Many breeds of dogs are sensitive to spe-cific anesthetics.

Reality—Although certain breeds may be predis-posed to problems that affect their responses to anesthe-sia (eg, cardiomyopathy in Doberman Pinschers andupper airway collapse in Bulldogs), very few breed-relat-ed sensitivities to anesthetic drugs have been identified.Greyhounds do have a well-documented tendency tohave prolonged recoveries from thiobarbiturate anesthe-sia.5,6 And by extrapolation, many veterinarians avoidthe use of thiopental in all sighthounds (eg, Whippets,

Afghan Hounds, and Borzois), although sighthoundsother than Greyhounds have not been studied in a con-trolled fashion and may not be similarly affected.

In addition, there are numerous anecdotal reportsof Boxers fainting or collapsing when given acepro-mazine, possibly from excessive vagal response.Although poorly documented, this phenomenon seemsto follow a geographic distribution, being more com-monly reported in England, which may indicate a famil-ial or genetic component. The authors have adminis-tered acepromazine at doses of 0.01 to 0.04 mg/kg(0.005 to 0.018 mg/lb), SC, to Boxers in Colorado with-out untoward effects, but recommend caution withdose and patient selection.

Finally, many veterinarians have a clinical impres-sion that dogs of northern breeds, such as AlaskanMalamutes, Siberian Huskies, and Samoyeds, tend torespond to opioid administration by vocalizing or evi-dencing dysphoric behavior. However, many northern-breed dogs respond appropriately to administration ofopioids at lower dosages or to administration of opi-oids concurrently with a tranquilizer.

In summary, although many dog owners believerumors that their particular breeds are sensitive to cer-tain anesthetic drugs or that certain anesthetic drugsare contraindicated in their breeds, there is little evi-dence to support most of these rumors.

Myth—Preanesthetic medications should not beused because they delay recovery.

Reality—Premedications are very valuable in mostcases. Tranquilizers, sedatives, and analgesics decreaseanxiety and pain associated with hospitalization,restraint, injections, and other unpleasant procedures.They decrease the required doses of induction drugsand gas anesthetics, frequently resulting in less cardio-vascular depression during induction and maintenanceof anesthesia.7-10 While it is true that some premedica-tions lead to prolonged sleepiness during recovery,most animals that have undergone painful proceduresbenefit from a quiet recovery period. After nonpainfulprocedures, the effects of some premedications (eg,opioids, benzodiazepines, and α2-adrenoceptor ago-nists) can be reversed or partially reversed, if necessary,to expedite recovery.11-15

Myth—Small doses of α2-adrenoceptor agonistshave minimal cardiovascular effects.

From the Department of Clinical Sciences, College of VeterinaryMedicine and Biomedical Sciences, Colorado State University, FortCollins, CO 80523.

Address correspondence to Dr. Wagner.

Myths and misconceptions in small animal anesthesia

Ann E. Wagner, DVM, MS, DACVA, DACVP; Bonnie D. Wright, DVM, DACVA; Peter W. Hellyer, DVM, MS, DACVA

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Reality—While the manufacturer of medetomidine,an α2-adrenoceptor agonist, has recommended16 the useof doses ranging from 18 to 71 µg/kg (8.2 to 32.3 µg/lb),IV, much lower doses (1 to 10 µg/kg [0.45 to 4.5 µg/lb],IV) are sometimes useful to provide short-term sedationand analgesia. However, it has been reported that admin-istration of medetomidine at a dose of 1 µg/kg, IV, in dogscaused cardiac output to decrease to < 40% of resting val-ues and to remain nearly 50% below normal for at leastan hour.17 In healthy young animals with good cardio-vascular function, this decrease may be tolerated, but inolder animals and animals with preexisting cardiac dis-ease, such a decrease may have deleterious effects on tis-sue perfusion and oxygen delivery, including reducedperfusion of the myocardium itself. Interestingly, severalsurveys of small animal veterinary practices have sug-gested that use of the α2-adrenoceptor agonist xylazine isassociated with a higher incidence of perianesthetic com-plications or death than use of any other anesthetic drug,possibly related to its detrimental cardiovascular effects.1,3

Although α2-adrenoceptor agonists can induce excellentsedation and analgesia, caution is advised with regard topatient selection, even when very low doses are used.

Myth—The fewer drugs used to anesthetize ananimal, the safer.

Reality—Actually, balanced anesthesia techniquesthat involve administration of multiple drugs oftenallow smaller doses of each drug to be used, resultingin fewer or less profound adverse effects than when alarge dose of a single drug is used. For instance, theinduction dose of propofol in dogs premedicated withacepromazine is about half the induction dose neededin dogs that have not been premedicated.18 Morphineadministration can decrease the minimum alveolarconcentration (MAC) of gas anesthetics by up to63%.10 The use of balanced anesthetic techniques thatinvolve lower doses of relatively depressant drugs,such as gas anesthetics, which produce profound dose-dependent hypotension, may benefit many patients.

Myth—It is dangerous to use more than 1 type ofanalgesic at a time in an animal.

Reality—Prevention and treatment of pain shouldinvolve a multimodal or balanced technique similar tothe balanced techniques used for anesthesia.19-21 Drugsused to provide perioperative analgesia include opi-oids, α2-adrenoceptor agonists, local anesthetics, non-steroidal anti-inflammatory drugs, and ketamine. Thegoal of using more than 1 drug is to provide better paincontrol while minimizing adverse effects. Single drugtechniques can be used effectively to treat minor painin dogs and cats. Acute pain induced by trauma orsurgery generally responds better to combination drugtherapy, rather than single drug treatment, in partbecause analgesics from different classes exert theireffects in different parts of the neuroanatomic path-ways giving rise to pain. Thus, combining 2 or moreanalgesic drugs during the perioperative period mayprovide additive or synergistic analgesic effects.

Myth—Opioids are dangerous because of theirpotential for adverse effects.

Reality—The adverse effects associated with opi-oids administered during the perioperative period indogs and cats are rarely serious. The respiratorydepressant effects of opioids in dogs and cats are muchless profound than the effects in people, although someanesthetized animals given opioids along with otherrespiratory depressant induction drugs and gas anes-thetics do benefit from mechanical ventilation.22

Hypoxemia may accompany respiratory depression ifoxygen is not supplemented. Vomiting and defecationmay occur when nonpainful animals are given an opi-oid, such as a preanesthetic dose of morphine, but usu-ally this is a 1-time occurrence that does not seem to bea problem in the postoperative period or when opioidsare given to an animal experiencing pain. Opioids caninterfere with thermoregulation, but if necessary, bodytemperature can usually be maintained with appropri-ate heating or cooling devices. Behavioral changes,which can include agitation and dysphoria or excessivesedation, may occur in conscious animals treated withopioids; however, these effects can usually be managedby adjusting the opioid dosage, administering a tran-quilizer concurrently, or administering a partial antag-onist. Some of the advantages of using opioids areexcellent analgesia, minimal cardiovascular depressanteffects, ability to decrease doses of other anestheticdrugs such as gas anesthetics, and ability to be reversedor antagonized.

Myth—Butorphanol is an effective and long-last-ing analgesic.

Reality—A study of female dogs undergoingovariohysterectomy found that administration ofbutorphanol at a dose of 0.5 mg/kg (0.23 mg/lb), IM,did not provide complete analgesia in all dogs at anytime, and all dogs had signs of incisional pain by 30to 90 minutes after receiving butorphanol.23 For vis-ceral pain (colon balloon model), butorphanol at adose of 0.4 mg/kg (0.18 mg/lb), SC, produced anal-gesia for < 60 minutes, even though a dose of 0.4mg/kg was considered optimum, with a ceiling effectoccurring at doses > 0.8 mg/kg (0.36 mg/lb).24 Inanother study,25 butorphanol did not significantlychange the MAC of halothane in dogs. Taken togeth-er, these data suggest that butorphanol is useful onlyfor fairly mild pain and if used for pain control indogs, it should be administered every 1 to 2 hours.In cats undergoing onychectomy, butorphanoladministration improved analgesia.26 However, theefficacy of butorphanol in cats varies widely, as doesthe duration of its effects, which have been reportedto be from 80 to 360 minutes.27

Myth—Induction of anesthesia with gas anesthet-ics is safer than induction with injectable anesthetics.

Reality—Struggling and excitement during maskinduction are not only unpleasant for the patient anddangerous for personnel, but may also lead to higherserum catecholamine concentrations, which can pre-dispose to arrhythmias and anesthetic overdose.Induction times with gas anesthetics, even with newer,less-soluble anesthetics such as sevoflurane, are slowerthan induction times with injectable anesthetics. A

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recent studya of cats reported that mean ± SD times tointubation with sevoflurane and isoflurane inductionwere 7.2 ± 1.1 and 8.6 ± 1.2 minutes, respectively. Bycomparison, most IV induction techniques allow intu-bation within 1 or 2 minutes. During the relatively pro-longed induction period necessary with gas anesthet-ics, there is no airway control, and hypoventilation canbe severe, especially in patients with preexisting respi-ratory compromise such as a collapsing trachea ordiaphragmatic hernia. In addition, the depth of anes-thesia required for endotracheal intubation of a patientis usually about 30% greater than that required for sur-gical incision,28 which means that by the time mostpatients are intubated following mask induction, theywill have already experienced considerable cardiovas-cular and respiratory depression. At least 1 privatepractice has found that hypotension (systolic arterialblood pressure < 90 mm Hg) occurred more frequent-ly in dogs and cats in which anesthesia was inducedwith an inhalant anesthetic delivered by mask (37%),compared with those in which anesthesia was inducedwith injectable drugs (14%).b In addition, the highoxygen flows and vaporizer settings required for gasinduction are wasteful and result in substantial pollu-tion that contributes to occupational health hazards.

Myth—Thiopental is a dangerous and outdatedanesthetic induction drug.

Reality—Thiopental is a reliable and economicalinduction agent that still has a place in veterinary anes-thesia. Thiopental is chemically stable and resists bac-terial growth for up to 4 weeks.29 Anesthetic inductionwith thiopental is usually rapid, smooth, and excite-ment-free. In healthy dogs, thiopental may increaseheart rate and decrease stroke volume, resulting in lit-tle change in blood pressure or cardiac output.Reducing the induction dose of thiopental by adminis-tering premedications reduces the cardiovasculareffects.30 Ventricular dysrhythmias can occur withthiopental, but these too are less common whenadministration of premedications allows lower doses ofthiopental to be used.31 Clinical impressions suggestthat supplementing oxygen prior to and during induc-tion also seems to reduce the incidence of dysrhyth-mias. A study of the use of thiopental in hypovolemicdogs concluded that thiopental had minimal deleteri-ous effects, most cardiovascular variables improved,and neither hypotension nor respiratory depressionoccurred.32 Nonpremedicated dogs recovering fromthiopental alone may be groggy and have difficultystanding, but tranquilizers or opioids generally help tosmooth recovery, as does a period of gas anesthesia.

Myth—Acepromazine-ketamine is a good combi-nation for surgical anesthesia in cats.

Reality—A combination of acepromazine and ket-amine has commonly been used as a general anesthet-ic in cats undergoing routine procedures such as ovar-iohysterectomy, castration, and onychectomy.Acepromazine is a tranquilizer and provides no analge-sia, whereas ketamine is generally thought to providegood superficial analgesia and little to no analgesia for

deep or visceral pain. Administration of acepromazine(0.11 mg/kg [0.05 mg/lb], IM) and atropine (0.045 to0.067 mg/kg [0.02 to 0.03 mg/lb], IM) 15 minutesprior to administration of ketamine (22 mg/kg [10mg/lb], IM) has been used in cats to provide anesthe-sia for surgical procedures.33 Another combinationcited includes acepromazine (0.2 mg/kg [0.09 mg/lb],IM), butorphanol (0.4 mg/kg, IM), and ketamine (25mg/kg [11.4 mg/lb], IM) for elective procedures suchas ovariectomy. Thus, the doses of ketamine used toprovide analgesia and general anesthesia are relativelyhigh. Lower doses of ketamine, which are frequentlyused to induce anesthesia in dogs and cats, are unlike-ly to provide anesthesia sufficient for surgical proce-dures. Higher doses of ketamine increase the risk ofadverse cardiovascular effects, such as tachycardia,hypertension, and the associated increase in myocar-dial oxygen demand, and are more likely to be associ-ated with prolonged and rough recoveries.Acepromazine and ketamine administered withoutsupplemental oxygen increases the risk of anesthesia-related hypoxemia. Ketamine-induced CNS and car-diovascular stimulation may be particularly detrimen-tal in the presence of hypoxemia. Although both ace-promazine and ketamine are useful anesthetic drugs incats, inducing and maintaining anesthesia with thiscombination places cats at undue risk for inadequateanalgesia and clinically important adverse effects.

Myth—Ketamine is a safe drug in patients withfailing cardiac function.

Reality—Ketamine is considered to be a relativelysafe induction drug, with a therapeutic index (ie, theratio of median lethal dose to median effective dose) of8.5 to 16, depending on species, compared withthiopental’s therapeutic index of 4.6 to 7.34 In addition,in a survey of small animal veterinarians in Colorado,ketamine was the most popular induction drug.35

When used in healthy patients without other medica-tions, ketamine generally increases heart rate andblood pressure as a result of a generalized increase insympathetic tone. However, in isolated heart prepara-tions, the direct effect of ketamine on the myocardiumis depression.36 In patients with clinically importantcardiac disease, patients in shock that have sympathet-ic neurotransmitter depletion, and patients in whichketamine is used concurrently with other drugs such asbenzodiazepines, the sympathomimetic, cardiostimu-latory effects of ketamine are not apparent and cardiacdepression may ensue.37 Therefore, although ketamineis an excellent induction drug in many situations andmay have additional benefits in regard to pain relief,caution is advised with its use in patients with heartfailure.

Myth—Propofol is the safest injectable anestheticinduction drug.

Reality—The therapeutic index of propofol is sim-ilar to that of thiopental, and both are probably slight-ly less safe, in this regard, than ketamine.34 Anincreased incidence of postoperative infections hasbeen associated with use of propofol, possibly as a

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result of suppression of reticuloendothelial function bythe diluent.38 Cardiorespiratory effects of propofol aresimilar to those of thiopental, although propofol is lesslikely to increase heart rate or induce arrhythmias.39

Because the blood-brain equilibrium time for propofolis about 3 minutes, compared with 1 minute for mostother induction drugs, it may be easier to overdose ani-mals with propofol than with other faster-acting induc-tion drugs. In dogs, propofol can induce substantialvasodilation,34 and at the Colorado State UniversityVeterinary Teaching Hospital, hypotension is such acommon sequela to propofol induction that a bolus offluids (5 to 10 mL/kg [2.3 to 4.5 mL/lb]) is adminis-tered IV to almost all patients before propofol is given.Cyanosis is also reported with propofol inductionunless oxygen is supplemented before, during, andafter induction.34 Propofol’s biggest advantage is therapid, smooth recovery associated with its use, and thisis certainly a reason to prefer propofol for short out-patient procedures in appropriately selected patients.

Myth—Sevoflurane is superior to isoflurane, andyou are out of date if you are not using sevoflurane.

Reality—While everyone is entitled to his or herpersonal preferences, there is no compelling reason toswitch from isoflurane to sevoflurane. Sevoflurane andisoflurane induce similar dose-related cardiovascularand respiratory depression,40 and neither drug sensi-tizes the heart to catecholamine-induced arrhythmias.Although the lower solubility of sevoflurane shouldresult in faster induction and recovery times, a recentstudya in cats demonstrated that induction was onlyslightly faster when sevoflurane was used (mean, 7.2min), compared with isoflurane (mean, 8.6 min), andrecovery time was not significantly different betweenthe 2 drugs. In addition, isoflurane does not producetoxic by-products. Although clinical use of sevofluranehas not been associated with increased renal toxicoses,sevoflurane breakdown can produce fluoride ions andsmall amounts of compound A, which have the poten-tial to be toxic to the kidneys.41 Therefore, low oxygenflow rates (< 1 to 2 L/min) are not recommended whenusing sevoflurane. Currently, sevoflurane is consider-ably (approx 5 times) more expensive than isoflurane.

Myth—Intravenous administration of fluids iswarranted only during long surgical procedures.

Reality—Fluids are administered IV to compen-sate for insensible fluid losses that occur during anes-thesia and surgery. Fluid loss is generally attributed todrying of exposed tissues and evaporation from the res-piratory tract, especially with the administration ofoxygen. Longer surgical procedures have a greaterpotential than shorter procedures for clinically signifi-cant fluid losses to occur. Nevertheless, IV administra-tion of fluids is also beneficial in patients anesthetizedfor short procedures. As discussed elsewhere in thistext, dogs and cats anesthetized for short, routine pro-cedures are at risk of hypotension. The withholding offood prior to anesthesia, coupled with the reluctance ofsome dogs and cats to drink water while at a veterinaryclinic, may lead to dehydration prior to anesthesia.Even mild degrees of dehydration, which tend to be

difficult to recognize clinically, increase the likelihoodof hypotension during anesthesia. Intravenous admin-istration of fluids is 1 of the cornerstones of preventingand treating hypotension during anesthesia.

Intravenous administration of fluids may decreaserecovery time by helping to maintain hepatic and renalblood flow, thereby hastening the elimination of anes-thetic drugs. A return to normal function after anesthe-sia may be slowed by dehydration, which may actuallybecome worse during recovery if the animal is still notdrinking. Overall, IV administration of fluids preventsand corrects dehydration and hypotension and facili-tates the elimination of anesthetic drugs, all of which areas important with a short procedure as with a long one.Finally, placing an IV catheter provides venous accessfor administration of emergency drugs in the event of anuntoward episode during anesthesia and surgery.

Myth—Electrocardiographic activity indicates abeating heart.

Reality—While ECG monitoring is useful indetecting changes in heart rate or rhythm, it should berecognized that the ECG indicates electrical activityonly, not mechanical activity (pumping) by the heartmuscle. It is possible to have relatively normal ECGactivity concurrently with severe hypotension or evencardiac arrest, as evidenced by continuation of ECGactivity for several minutes following administration ofan overdose of pentobarbital for euthanasia. Therefore,the ECG alone should not be relied on to indicate thecirculatory status of an anesthetized patient.

Myth—Respiratory depression or apnea duringanesthesia is a crisis.

Reality—Apnea is rarely a crisis unless the animalcannot be intubated. Most anesthetized, intubated ani-mals breathing 100% oxygen can remain adequately oxy-genated with only 1 or 2 breaths/min.42 Pulse oximetrycan help determine whether oxygenation is adequate,and capnography or measurement of arterial blood gaspartial pressures, if available, can confirm severe respira-tory depression. If excessive respiratory depression orapnea occurs, efforts should be made to identify and cor-rect the cause (eg, excessive anesthetic depth, recentadministration of a respiratory depressant drug, andiatrogenic hyperventilation). In the meantime, providing1 to 2 breaths/min of 100% oxygen will sustain adequateoxygenation in most patients, although hypercapnia maypersist or worsen. Animals that cannot be expected tobreathe spontaneously (eg, animals with a diaphragmat-ic hernia or undergoing an open chest procedure) andanimals in which hypercapnia would be particularlydetrimental (eg, animals with a brain tumor or head trau-ma) should be manually or mechanically ventilated at arate of 8 to 15 breaths/min to help maintain normal oxy-gen and carbon dioxide partial pressures.

Myth—Pulse oximeters measure the adequacy ofventilation during inhalant anesthesia.

Reality—During inhalant anesthesia, oxygen isalmost always used as the carrier gas and often com-prises > 90% of the total inspired gases. As stated pre-

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viously, at this concentration of oxygen, even completeapnea will not result in hypoxemia in dogs and catswith normal lung function for upwards of 30 minutes(although this time is less in horses).42,43 Therefore,pulse oximetry cannot be expected to detect hypoven-tilation in oxygen-breathing patients. In patientsbreathing room air (21% oxygen), however, desatura-tion generally accompanies hypoventilation and pulseoximetry may be useful in indicating hypoventilation-induced hypoxemia in these patients.44

Myth—A strong palpable pulse indicates goodblood pressure and perfusion.

Reality—While a palpable pulse does at least con-firm that the heart is beating and creating some degreeof circulation, a strong pulse indicates only that thereis a large difference between systolic and diastolicblood pressures, not necessarily an optimal meanblood pressure or good perfusion of tissues.45 Forexample, a puppy with a patent ductus arteriosus mayhave exceptionally strong pulses, yet have low meanblood pressure and relatively poor tissue perfusion.Many anesthetized animals with palpably normal puls-es are actually hypotensive, as indicated by mean arte-rial blood pressure < 70 mm Hg.

Myth—I would know if my anesthetized patientshad low blood pressure.

Reality—As indicated previously, the only way toaccurately assess blood pressure is to measure it. Manyanimals that are hypotensive during anesthesia appearclinically normal, with normal heart and respiratoryrates, pink mucous membranes, and physical signs(eye position and reflexes and jaw tone) indicatingappropriate anesthetic depth. When asked to name thebiggest problem encountered when anesthetizing dogsand cats, only 1 of more than 20 small animal veteri-narians interviewed cited hypotension; it is unlikely tobe purely coincidental that the same veterinarian wasalso the only one in the group who routinely measuredblood pressure in her anesthetized patients.46 Manydogs and cats that are hypotensive appear to recoverfrom anesthesia without any overt problems. However,vital organs such as the kidneys, which require a min-imum blood pressure to maintain adequate perfusion,can be damaged by hypotension. Because 75% ofnephrons must be nonfunctional before BUN and cre-atinine concentrations increase or clinical signs appear,it is likely that substantial perianesthetic kidney dam-age might go unnoticed. At least 1 expert on renal dis-ease has suggested that measurement of arterial bloodpressure during anesthesia would help reduce the like-lihood of renal ischemia.47

Myth—Low blood pressure during anesthesia onlyhappens to old or sick animals.

Reality—At the Colorado State UniversityVeterinary Teaching Hospital, blood pressure is routine-ly measured in all anesthetized animals. A recent surveyof 1 year’s anesthesia records indicated that 32% of allanesthetized dogs were hypotensive (systolic arterialpressure < 90 mm Hg or mean arterial pressure

< 60 mm Hg) at some point during anesthesia. It mightbe speculated that the patients anesthetized in academ-ic veterinary hospitals tend to be sicker and thereforemore susceptible to anesthetic-induced hypotensionthan those anesthetized in private practices for routineelective surgeries. However, a separate review ofVeterinary Teaching Hospital patients undergoing onlyelective ovariohysterectomy indicated that 28% of thesepresumably healthy and young dogs were hypotensive.Given that all of these patients were administered fluidsIV at a standard rate of 5 to 10 mL/kg/h during anes-thesia, it is likely that the incidence of hypotensionmight have been even higher if fluids had not beengiven. In most cases, hypotension was corrected bydecreasing the anesthetic vaporizer setting or adminis-tering additional fluids IV, but in 12% of anesthetizeddogs, inotropes such as dobutamine or ephedrine hadto be administered to increase blood pressure to anacceptable value. A separate survey of blood pressuremeasurements in a private small animal veterinary clin-ic indicated that hypotension occurred in 22% of anes-thetized dogs and 33% of anesthetized cats for an over-all incidence of 27%.b In that clinic, blood pressureincreased when the vaporizer setting was decreased (6%of anesthetized animals) or when additional fluids wereadministered IV (8% of anesthetized animals), but 13%of all anesthetized animals were hypotensive and didnot receive any treatment.b

Myth—Dentistry is a minor procedure thatrequires no special patient preparation or monitoringduring anesthesia.

Reality—Many patients that undergo dental pro-cedures are old and have other problems such as mitralregurgitation or hepatic or renal disease. Consequently,anesthesia of these patients is likely to entail greaterrisk than anesthesia of younger, healthier patients, andthe anesthetic protocol should be planned only aftercareful consideration of physical examination and lab-oratory findings. Appropriate IV administration of flu-ids and monitoring of blood pressure, oxygenation,and heart rate and rhythm are especially important inolder or compromised patients.

Myth—Bradycardia is a sign that the vaporizer set-ting should be decreased.

Reality—Although tachycardia during surgicalstimulation may indicate an insufficient plane of anes-thesia, deep planes of gas anesthesia as a general ruledo not cause bradycardia. Increasing the depth of anes-thesia with some anesthetics, such as sevoflurane, mayactually cause the heart rate to increase.48 Bradycardiaduring anesthesia is more often associated with the useof opioids and α2-adrenoceptor agonists or with inter-ventions that increase vagal tone (usually responsive toanticholinergics) or hypothermia (often unresponsiveto anticholinergics).

Myth—Movement during anesthesia indicatesconscious awareness by the patient.

Reality—One of the important benefits of generalanesthesia is its ability to render a patient immobile.

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Immobility is helpful in many procedures and vital ina few. The MAC of an inhalant anesthetic, the primaryindicator of its anesthetic potency, is defined as theMAC required to prevent movement in response to anoxious stimulus in 50% of the patients studied. Ingeneral, muscle activity is reduced in a linear fashionas anesthetic depth is increased.49 For these reasons,immobility is generally regarded as an important mark-er of anesthetic depth. However, when cerebral func-tion is studied, the onset of movement is not closelyassociated with the onset of consciousness. In fact, afair amount of movement can occur long before aware-ness is reported in people.50,51 Therefore, movementthat does not interfere with the procedures being per-formed may not be detrimental to the patient. Anunderstanding of this fact may prevent an overreactionto movements during anesthesia and prevent anes-thetizing patients beyond what is necessary, leading tocardiovascular and respiratory depression, which maybe far more detrimental.

Myth—Animals that take a long time to wake upwere probably at too high a vaporizer setting.

Reality—Currently used anesthetics, such asisoflurane and sevoflurane, are relatively quickly elim-inated through the respiratory system once the vapor-izer is turned off, and extubation should be achievedwithin 10 minutes.a For animals on a circle system,periodically emptying the rebreathing bag and refillingit with pure oxygen will help prevent rebreathing of theanesthetic. Even after deep levels of anesthesia, theblood and brain concentrations of gas anestheticsshould decrease sufficiently within 15 minutes that theanimal will wake up. If it does not, other potentialcauses of prolonged anesthesia, such as hypothermiaand administration of sedative drugs such as opioids,should be considered. It is important to realize that afast recovery is not necessarily a good recovery; ani-mals that have undergone pain-inducing proceduresare likely to benefit from both the analgesia and slow-er, quieter recovery afforded by administration of opi-oids.

Myth—Administering oxygen at the end ofsurgery delays recovery.

Reality—The administration of oxygen has mini-mal to no effect on recovery time but may have bene-fits in preventing hypoxemia. Discontinuation of oxy-gen administration before extubation resulted inhypoxemia (pulse oximeter values < 90%) within 3minutes in 5% of healthy dogs (American Society ofAnesthesiologists status 1 or 2) recovering from anes-thesia.c If a circle system is used, periodically emptyingthe breathing bag and refilling it with oxygen will helpremove exhaled anesthetic from the system. Assuminga scavenging system is in use, keeping the animal con-nected to the anesthesia breathing circuit during recov-ery has the added benefit of reducing pollution in therecovery area.

Myth—I would know if my patients were in painafter surgery.

Reality—Recognizing pain in the postoperative

period is often difficult in dogs and cats.52-54 Somepainful dogs and cats will display behaviors that willbe correctly interpreted as pain. Unfortunately, manyother animals will not demonstrate behaviors thatwill convince the veterinary staff that are actually inpain. In fact, residual anesthetic drugs and tranquil-izers such as acepromazine often prevent or mask thedemonstration of behaviors suggestive of pain.Adding to the difficulty of recognizing pain is thefact that no foolproof method exists to measure andquantify pain in animals.

Diagnosing pain in animals often requires timeand knowledge of the normal behavior of the speciesand individual. It is certainly understandable that abusy veterinary staff with no training in the evaluationof pain would frequently overlook painful patients.Since the correct diagnosis of pain in dogs and cats isoften difficult, a working assumption that all surgicalprocedures inflict pain in animals will provide betterquality of care than the assumption that the staff willbe able to readily recognize those animals in need ofanalgesics. Proactively using analgesics to minimizepostoperative pain is consistent with the fundamentalprinciples of providing good medical care to each ofour patients.

aAmai A, Steffey EP, Ilkiw JE, et al. Quantitative characteristics of anes-thetic induction with and recovery from isoflurane and sevoflurane incats (abstr), in Proceedings. Annu Meet Am Coll Vet Anesth 2002;47.

bGordon A, Westarbor Animal Hospital, Ann Arbor, Mich: Personalcommunication, 2003.

cGaynor JS, Animal Emergency Care Center North, ColoradoSprings, Colo: Personal communication, 2003.

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