Objective—To compare the disposition of lidocaine
administered IV in awake and anesthetized horses.
Procedure—After instrumentation and collection of
baseline data, lidocaine (loading infusion, 1.3 mg/kg
administered during 15 minutes (87 µg/kg/min); constant
rate infusion, 50 µg/kg/min) was administered IV
to awake or anesthetized horses for a total of 105 minutes.
Blood samples were collected at fixed times during
the loading and maintenance infusion periods and
after the infusion period for analysis of serum lidocaine
concentrations by use of liquid chromatography with
mass spectral detection. Selected cardiopulmonary
parameters including heart rate (HR), mean arterial
pressure (MAP), arterial pH, PaCO2, and PaO2 were also
recorded at fixed time points during lidocaine administration.
Serum lidocaine concentrations were evaluated
by use of standard noncompartmental analysis.
Results—Serum lidocaine concentrations were higher
in anesthetized than awake horses at all time points
during lidocaine administration. Serum lidocaine concentrations
reached peak values during the loading
infusion in both groups (1,849 ± 385 ng/mL and
3,348 ± 602 ng/mL in awake and anesthetized horses,
respectively). Most lidocaine pharmacokinetic variables
also differed between groups. Differences in cardiopulmonary
variables were predictable; for example,
HR and MAP were lower and PaO2 was higher in anesthetized
than awake horses but within reference
ranges reported for horses under similar conditions.
Conclusions and Clinical Relevance—Anesthesia
has an influence on the disposition of lidocaine in horses,
and a change in dosing during anesthesia should
be considered. (Am J Vet Res 2005;66:574–580)
Objective—To measure cardiac output in healthy
female anesthetized dogs by use of lithium dilution
cardiac output and determine whether changes in
mean arterial pressure were caused by changes in
cardiac output or systemic vascular resistance.
Design—Prospective clinical study.
Animals—20 healthy female dogs.
Procedure—Dogs were anesthetized for ovariohysterectomy.
Ten dogs breathed spontaneously throughout
anesthesia, and 10 dogs received intermittent
positive-pressure ventilation. Cardiovascular and respiratory
measurements, including lithium dilution cardiac
output, were performed during anesthesia and
Results—Mean arterial pressure and systemic vascular
resistance index were low after induction of
anesthesia and just prior to surgery and increased
significantly after surgery began. Cardiac index (cardiac
output indexed to body surface area) did not
change significantly throughout anesthesia and
Conclusions and Clinical Relevance—Results provide
baseline data for cardiac output and cardiac index
measurements during clinical anesthesia and surgery
in dogs. Changes in mean arterial pressure do not
necessarily reflect corresponding changes in cardiac
index. (J Am Vet Med Assoc 2005;227:1419–1423)
Objective—To measure cardiac output and other hemodynamic variables in anesthetized dogs undergoing laparotomy because of abdominal neoplasia.
Design—Prospective case series.
Animals—8 dogs with splenic or hepatic tumors.
Procedures—Dogs were anesthetized and underwent abdominal laparotomy. End-tidal isoflurane concentration, heart rate, arterial blood pressures, cardiac output, arterial pH, blood gas partial pressures, PCV, and plasma total protein concentration were measured at set intervals before, during, and after surgery. Cardiac index, stroke index, and systemic vascular resistance index were calculated.
Results—End-tidal isoflurane concentration was lowest before and after surgery. Heart rate did not change significantly throughout the anesthetic period. Arterial blood pressures and systemic vascular resistance index were highest shortly after surgery began; cardiac index and stroke volume index did not change significantly during surgery but increased significantly after surgery ended.
Conclusions and Clinical Relevance—Results suggested that in dogs undergoing laparotomy because of abdominal neoplasia, changes in arterial blood pressures were not necessarily indicative of qualitatively similar changes in cardiac index.
Objective—To determine whether infusion of xylazine and ketamine or xylazine and propofol after sevoflurane administration in horses would improve the quality of recovery from anesthesia.
Animals—6 healthy adult horses.
Procedures—For each horse, anesthesia was induced by administration of xylazine, diazepam, and ketamine and maintained with sevoflurane for approximately 90 minutes (of which the last 60 minutes were under steady-state conditions) 3 times at 1-week intervals. For 1 anesthetic episode, each horse was allowed to recover from sevoflurane anesthesia; for the other 2 episodes, xylazine and ketamine or xylazine and propofol were infused for 30 or 15 minutes, respectively, after termination of sevoflurane administration. Selected cardiopulmonary variables were measured during anesthesia and recovery. Recovery events were monitored and subjectively scored.
Results—Cardiopulmonary variables differed minimally among treatments, although the xylazine-propofol infusion was associated with greater respiratory depression than was the xylazine-ketamine infusion. Interval from discontinuation of sevoflurane or infusion administration to standing did not differ significantly among treatments, but the number of attempts required to stand successfully was significantly lower after xylazine-propofol infusion, compared with the number of attempts after sevoflurane alone. Scores for recovery from anesthesia were significantly lower (ie, better recovery) after either infusion, compared with scores for sevoflurane administration alone.
Conclusions and Clinical Relevance—Xylazine-ketamine or xylazine-propofol infusion significantly improved quality of recovery from sevoflurane anesthesia in horses. Xylazine-ketamine or xylazine-propofol infusions may be of benefit during recovery from sevoflurane anesthesia in horses for which a smooth recovery is particularly critical. However, oxygenation and ventilation should be monitored carefully.
Objective—To evaluate the sedative and analgesic effects of subanesthetic doses of ketamine in horses sedated with xylazine, with or without butorphanol.
Design—Prospective, randomized, controlled study.
Animals—10 adult horses.
Procedures—Each horse was sedated multiple times by administration of xylazine (treatment X), xylazine and butorphanol (treatment XB), xylazine with 1 of 2 dosages of ketamine (treatment XK1 or XK2), or xylazine and butorphanol with 1 of 2 dosages of ketamine (treatment XBK1 or XBK2). Head height and various behaviors, including responses to noise, insertion of a dental float, needle prick on the flank, algometer pressure on the scapula, and bilateral carpal arthrocenteses, were evaluated.
Results—No significant differences were detected among sedation treatments for head height, response to noise, or response to arthrocenteses. Insertion of a dental float was easiest with treatment XBK2 and most difficult with treatments XK1 and XK2. Response to a needle prick on the flank was lowest with treatment XB and highest with treatment XK2. Tolerance to algometer pressure over the scapula was highest with treatment XBK2 and lowest with treatment X.
Conclusions and Clinical Relevance—Administration of a subanesthetic dosage of ketamine with xylazine and butorphanol may facilitate certain procedures, such as insertion of a dental float, in horses and enhance tolerance to pressure stimulation, but it may worsen responses to acute pain, such as that caused by a needle prick. Further evaluation is needed to determine whether subanesthetic dosages of ketamine might be useful when performing certain clinical procedures in horses.
Procedure—Lidocaine hydrochloride (loading infusion, 1.3 mg/kg during a 15-minute period [87.5 μg/kg/min]; maintenance infusion, 50 μg/kg/min for 60 to 90 minutes) was administered IV to dorsally recumbent anesthetized horses. Blood samples were collected before and at fixed time points during and after lidocaine infusion for analysis of serum drug concentrations by use of liquid chromatography-mass spectrometry. Serum lidocaine concentrations were evaluated by use of standard noncompartmental analysis. Selected cardiopulmonary variables, including heart rate (HR), mean arterial pressure (MAP), arterial pH, PaCO2, and PaO2, were recorded. Recovery quality was assessed and recorded.
Results—Serum lidocaine concentrations paralleled administration, increasing rapidly with the initiation of the loading infusion and decreasing rapidly following discontinuation of the maintenance infusion. Mean ± SD volume of distribution at steady state, total body clearance, and terminal half-life were 0.70 ± 0.39 L/kg, 25 ± 3 mL/kg/min, and 65 ± 33 minutes, respectively. Cardiopulmonary variables were within reference ranges for horses anesthetized with inhalation anesthetics. Mean HR ranged from 36 ± 1 beats/min to 43 ± 9 beats/min, and mean MAP ranged from 74 ± 18 mm Hg to 89 ± 10 mm Hg. Recovery quality ranged from poor to excellent.
Conclusions and Clinical Relevance—Availability of pharmacokinetic data for horses with gastrointestinal tract disease will facilitate appropriate clinical dosing of lidocaine.
Objective—To determine the effect of a constant-rate
infusion of fentanyl on minimum alveolar concentration
(MAC) of isoflurane and to determine the interaction
between fentanyl and a benzodiazepine agonist
(diazepam) and antagonist (flumazenil) in isoflurane-anesthetized
Animals—8 mixed-breed adult dogs.
Procedure—Dogs were anesthetized with isoflurane
3 times during a 6-week period. After a 30-minute
equilibration period, each MAC determination was
performed in triplicate, using standard techniques.
Fentanyl was administered as a bolus (10 µg/kg of
body weight, IV) that was followed by a constant infusion
(0.3 µg/kg per min, IV) throughout the remainder
of the experiment. After determining isoflurane-fentanyl
MAC in triplicate, each dog received saline
(0.9% NaCl) solution, diazepam, or flumazenil. After
30 minutes, MAC was determined again.
Results—Fentanyl significantly decreased isoflurane
MAC (corrected to a barometric pressure of 760 mm
Hg) from 1.80 ± 0.21 to 0.85 ± 0.14%, a reduction of
53%. Isoflurane-fentanyl-diazepam MAC (0.48 ±
0.29%) was significantly less than isoflurane-fentanylsaline
MAC (0.79 ± 0.21%). Percentage reduction in
isoflurane MAC was significantly greater for fentanyldiazepam
(74%), compared with fentanyl-saline (54%)
or fentanyl-flumazenil (61%). Mean fentanyl concentrations
for the entire experiment were increased over
time and were higher in the diazepam group than the
saline or flumazenil groups.
Conclusion and Clinical Relevance—Fentanyl
markedly decreased isoflurane MAC in dogs.
Diazepam, but not flumazenil, further decreased
isoflurane-fentanyl MAC. Our results indicate that
diazepam enhances, whereas flumazenil does not
affect, opioid-induced CNS depression and, possibly,
analgesia in dogs. (Am J Vet Res 2001;62:555–560)