Objectives—To assess the effect of increasing serum
lithium concentrations on lithium dilution cardiac output
(LiDCO) determination and to determine the ability
to predict the serum lithium concentration from the
cumulative lithium chloride dosage.
Animals—10 dogs (7 males, 3 females).
Procedure—Cardiac output (CO) was determined in
anesthetized dogs by measuring LiDCO and thermodilution
cardiac output (TDCO). The effect of the
serum lithium concentration on LiDCO was assessed
by observing the agreement between TDCO and
LiDCO at various serum lithium concentrations. Also,
cumulative lithium chloride dosage was compared
with the corresponding serum lithium concentrations.
Results—44 paired observations were used. The linear
regression analysis for the effect of the serum
lithium concentration on the agreement between
TDCO and LiDCO revealed a slope of -1.530 (95%
confidence interval [CI], -2.388 to -0.671) and a yintercept
of 0.011 (r2 = 0.235). The linear regression
analysis for the effect of the cumulative lithium chloride
dosage on the serum lithium concentration
revealed a slope of 2.291 (95% CI, 2.153 to 2.429)
and a y-intercept of 0.008 (r2 = 0.969).
Conclusions and Clinical Relevance—The LiDCO
measurement increased slightly as the serum lithium
concentration increased. This error was not clinically
relevant and was minimal at a serum lithium concentration
of 0.1 mmol/L and modest at a concentration
of 0.4 mmol/L. The serum lithium concentration can
be reliably predicted from the cumulative lithium
dosage if lithium chloride is administered often within
a short period. (Am J Vet Res 2002;63:1048–1052)
Objective—To determine the pharmacokinetics and
toxic effects associated with IV administration of lithium
chloride (LiCl) to conscious healthy horses.
Animals—6 healthy Standardbred horses.
Procedure—Twenty 3-mmol boluses of LiCl (0.15
mmol/L) were injected IV at 3-minute intervals (total
dose, 60 mmol) during a 1-hour period. Blood samples
for measurement of serum lithium concentrations
were collected before injection and up to 24 hours
after injection. Behavioral and systemic toxic effects
of LiCl were also assessed.
Results—Lithium elimination could best be described
by a 3-compartment model for 5 of the 6 horses.
Mean peak serum concentration was 0.561 mmol/L
(range, 0.529 to 0.613 mmol/L), with actual measured
mean serum value of 0.575 mmol/L (range, 0.52 to
0.67 mmol/L) at 2.5 minutes after administration of the
last bolus. Half-life was 43.5 hours (range, 32 to 84
hours), and after 24 hours, mean serum lithium concentration
was 0.13 ± 0.05 mmol/L (range, 0.07 to
0.21 mmol/L). The 60-mmol dose of LiCl did not produce
significant differences in any measured hematologic
or biochemical variables, gastrointestinal motility,
or ECG variables evaluated during the study period.
Conclusions and Clinical Relevance—Distribution
of lithium best fit a 3-compartment model, and clearance
of the electrolyte was slow. Healthy horses
remained unaffected by LiCl at doses that exceeded
those required for determination of cardiac output.
Peak serum concentrations were less than steadystate
serum concentrations that reportedly cause
toxic effects in other species. (Am J Vet Res 2001;
Objective—To evaluate cardiopulmonary effects of
glycopyrrolate in horses anesthetized with halothane
Procedure—Horses were allocated to 2 treatment
groups in a randomized complete block design.
Anesthesia was maintained in mechanically ventilated
horses by administration of halothane (1% end-tidal
concentration) combined with a constant-rate
infusion of xylazine hydrochloride (1 mg/kg/h, IV).
Hemodynamic variables were monitored after induction
of anesthesia and for 120 minutes after administration
of glycopyrrolate or saline (0.9% NaCl) solution.
Glycopyrrolate (2.5 µg/kg, IV) was administered
at 10-minute intervals until heart rate (HR) increased
at least 30% above baseline or a maximum cumulative
dose of 7.5 µg/kg had been injected. Recovery
characteristics and intestinal auscultation scores
were evaluated for 24 hours after the end of anesthesia.
Results—Cumulative dose of glycopyrrolate administered
to 5 horses was 5 µg/kg, whereas 1 horse
received 7.5 µg/kg. The positive chronotropic effects
of glycopyrrolate were accompanied by an increase in
cardiac output, arterial blood pressure, and tissue oxygen
delivery. Whereas HR increased by 53% above
baseline values at 20 minutes after the last glycopyrrolate
injection, cardiac output and mean arterial pressure
increased by 38% and 31%, respectively.
Glycopyrrolate administration was associated with
impaction of the large colon in 1 horse and low intestinal
auscultation scores lasting 24 hours in 3 horses.
Conclusions and Clinical Relevance—The positive
chronotropic effects of glycopyrrolate resulted in
improvement of hemodynamic function in horses
anesthetized with halothane and xylazine. However,
prolonged intestinal stasis and colic may limit its use
during anesthesia. (Am J Vet Res 2004;65:456–463)
Objective—To evaluate cardiopulmonary effects of anesthetic induction with diazepam and ketamine or xylazine and ketamine, with subsequent maintenance of anesthesia with isoflurane, in foals undergoing abdominal surgery.
Animals—17 pony foals.
Procedures—Foals underwent laparotomy at 7 to 15 days of age and laparoscopy 7 to 10 days later. Foals were randomly assigned to receive diazepam, ketamine, and isoflurane (D/K/Iso; n = 8) or xylazine, ketamine, and isoflurane (X/K/Iso; 9) for both procedures.
Results—During anesthesia for laparotomy, cardiac index, and mean arterial blood pressure ranged from 110 to 180 mL/kg/min and 57 to 81 mm Hg, respectively, in the D/K/Iso group and 98 to 171 mL/kg/min and 50 to 66 mm Hg, respectively, in the X/K/Iso group. Cardiac index, heart rate, and arterial blood pressures were significantly higher in the D/K/Iso group, compared with the X/K/Iso group. During anesthesia for laparoscopy, cardiac index and mean arterial blood pressure ranged from 85 to 165 mL/kg/min and 67 to 83 mm Hg, respectively, in the D/K/Iso group, and 98 to 171 mL/kg/min and 48 to 67 mm Hg, respectively, in the X/K/Iso group. Heart rates and arterial blood pressures were significantly higher in the D/K/Iso group, compared with the X/K/Iso group. There were no significant differences between groups during either experimental period for percentage end-tidal isoflurane, arterial blood gas partial pressures, or pH values.
Conclusions and Clinical Relevance—Anesthesia of foals for abdominal surgery with D/K/Iso was associated with less hemodynamic depression than with X/K/Iso.
Objective—To evaluate the use of a lithium dilution
cardiac output (LiDCO) technique for measurement of
CO and determine the agreement between LiDCO and
thermodilution CO (TDCO) values in anesthetized cats.
Animals—6 mature cats.
Procedure—Cardiac output in isoflurane-anesthetized
cats was measured via each technique. To
induce different rates of CO in each cat, anesthesia
was maintained at > 1.5X end-tidal minimum alveolar
concentration (MAC) of isoflurane and at 1.3X endtidal
isoflurane MAC with or without administration of
dobutamine (1 to 3 µg/kg/min, IV). At least 2 comparisons
between LiDCO and TDCO values were made
at each CO rate. The TDCO indicator was 1.5 mL of
5% dextrose at room temperature; with the LiDCO
technique, each cat received 0.005 mmol of
lithium/kg (concentration, 0.015 mmol/mL). Serum
lithium concentrations were measured prior to the
first and following the last CO determination.
Results—35 of 47 recorded comparisons were analyzed;
via linear regression analysis (LiDCO vs TDCO
values), the coefficient of determination was 0.91.
The mean bias (TDCO-LiDCO) was –4 mL/kg/min (limits
of agreement, –35.8 to +27.2 mL/kg/min). The concordance
coefficient was 0.94. After the last CO
determination, serum lithium concentration was < 0.1
mmol/L in each cat.
Conclusions and Clinical Relevance—Results indicated
a strong relationship and good agreement
between LiDCO and TDCO values; the LiDCO
method appears to be a practical, relatively noninvasive
method for measurement of CO in anesthetized
cats. (Am J Vet Res 2005;66:1639–1645).
Objective—To evaluate the cardiopulmonary and sedative effects of the peripheral α2-adrenoceptor antagonist MK 0467 when administered IM or IV concurrently with medetomidine in dogs.
Animals—8 adult dogs.
Procedures—Dogs received 20 μg of medetomidine/kg, IM, alone or concurrently with MK 0467 (0.4 mg/kg, IM), and 10 μg of medetomidine/kg, IV, alone or concurrently with MK 0467 (0.2 mg/kg, IV), in a randomized crossover study. Sedation characteristics were scored and hemodynamic measurements and arterial and mixed-venous blood samples for blood gas analysis were obtained before (time 0; baseline) and for 90 minutes after treatment.
Results—Heart rate (HR), mixed-venous partial pressure of oxygen (Pvo2), and cardiac index (CI) were significantly lower and mean arterial blood pressure (MAP), systemic vascular resistance (SVR), and oxygen extraction ratio (ER) were significantly higher after administration of medetomidine IM or IV, compared with baseline values. Administration of medetomidine and MK 0467 IM caused a significantly higher heart rate, CI, and Pvo2 and significantly lower MAP, SVR, and ER for 60 to 90 minutes than did IM administration of medetomidine alone. Administration of medetomidine and MK 0467 IV caused a significantly higher CI and Pvo2 and significantly lower MAP, SVR, and ER for 45 to 90 minutes than did IV administration of medetomidine alone. There was no significant difference in sedation scores among treatments.
Conclusions and Clinical Relevance—In dogs, MK 0467 administered concurrently with medetomidine IV or IM reduced the cardiovascular effects of medetomidine but had no detectable effect on sedation scores.
Objective—To assess the sedative and cardiopulmonary effects of medetomidine and xylazine and their reversal with atipamezole in calves.
Procedures—A 2-phase (7-day interval) study was performed. Sedative characteristics (phase I) and cardiopulmonary effects (phase II) of medetomidine hydrochloride and xylazine hydrochloride administration followed by atipamezole hydrochloride administration were evaluated. In both phases, calves were randomly allocated to receive 1 of 4 treatments IV: medetomidine (0.03 mg/kg) followed by atipamezole (0.1 mg/kg; n = 6), xylazine (0.3 mg/kg) followed by atipamezole (0.04 mg/kg; 7), medetomidine (0.03 mg/kg) followed by saline (0.9% NaCl; 6) solution (10 mL), and xylazine (0.3 mg/kg) followed by saline solution (10 mL; 6). Atipamezole or saline solution was administered 20 minutes after the first injection. Cardiopulmonary variables were recorded at intervals for 35 minutes after medetomidine or xylazine administration.
Results—At the doses evaluated, xylazine and medetomidine induced a similar degree of sedation in calves; however, the duration of medetomidine-associated sedation was longer. Compared with pretreatment values, heart rate, cardiac index, and PaO2 decreased, whereas central venous pressure, PaCO2, and pulmonary artery pressures increased with medetomidine or xylazine. Systemic arterial blood pressures and vascular resistance increased with medetomidine and decreased with xylazine. Atipamezole reversed the sedative and most of the cardiopulmonary effects of both drugs.
Conclusions and Clinical Relevance—At these doses, xylazine and medetomidine induced similar degrees of sedation and cardiopulmonary depression in calves, although medetomidine administration resulted in increases in systemic arterial blood pressures. Atipamezole effectively reversed medetomidine- and xylazine-associated sedative and cardiopulmonary effects in calves.
Objective—To evaluate the cardiorespiratory and
intestinal effects of the muscarinic type-2 (M2) antagonist,
methoctramine, in anesthetized horses.
Procedure—Horses were allocated to 2 treatments
in a randomized complete block design. Anesthesia
was maintained with halothane (1% end-tidal concentration)
combined with a constant-rate infusion of
xylazine hydrochloride (1 mg/kg/h, IV) and mechanical
ventilation. Hemodynamic variables were monitored
after induction of anesthesia and for 120 minutes after
administration of methoctramine or saline (0.9%
NaCl) solution (control treatment). Methoctramine
was given at 10-minute intervals (10 µg/kg, IV) until
heart rate (HR) increased at least 30% above baseline
values or until a maximum cumulative dose of 30
µg/kg had been administered. Recovery characteristics,
intestinal auscultation scores, and intestinal transit
determined by use of chromium oxide were
assessed during the postanesthetic period.
Results—Methoctramine was given at a total cumulative
dose of 30 µg/kg to 4 horses, whereas 2 horses
received 10 µg/kg. Administration of methoctramine
resulted in increases in HR, cardiac output, arterial
blood pressure, and tissue oxygen delivery. Intestinal
auscultation scores and intestinal transit time (interval
to first and last detection of chromium oxide in the
feces) did not differ between treatment groups.
Conclusions and Clinical Relevance—Methoctramine
improved hemodynamic function in horses
anesthetized by use of halothane and xylazine without
causing a clinically detectable delay in the return
to normal intestinal motility during the postanesthetic
period. Because of their selective positive chronotropic
effects, M2 antagonists may represent a safe alternative
for treatment of horses with intraoperative
bradycardia. (Am J Vet Res 2004;65:464–472)
Objective—To assess accuracy and reliability of
open-flow indirect calorimetry in dogs.
Animals—13 clinically normal dogs.
Procedure—In phase 1, oxygen consumption per
kilogram of body weight (VO2kg) was determined in 6
anesthetized dogs by use of open-flow indirect
calorimetry before and after determination of VO2/kg
by use of closed-circuit spirometry. In phase 2, four
serial measurements of VO2 and carbon dioxide production
(VCO2) were obtained in 7 awake dogs by use
of indirect calorimetry on 2 consecutive days. Resting
energy expenditure (REE) was calculated.
Results—Level of clinical agreement was acceptable
between results of indirect calorimetry and spirometry.
Mean VO2/kg determined by use of calorimetry
before spirometry was significantly greater than that
obtained after spirometry. In phase 2, intraclass correlation
coefficients (ICC) for REE and VO2 were 0.779
and 0.786, respectively, when data from all 4 series
were combined. When the first series was discounted,
ICC increased to 0.904 and 0.894 for REE and VO2,
respectively. The most reliable and least variable measures
of REE and VO2 were obtained when the first 2
series were discounted.
Conclusions and Clinical Relevance—Open-flow
indirect calorimetry may be used clinically to obtain a
measure of VO2 and an estimate of REE in dogs. Serial
measurements of REE and VO2 in clinically normal
dogs are reliable, but a 10-minute adaption period
should be allowed, the first series of observations
should be discounted, multiple serial measurements
should be obtained, and REE. (Am J Vet Res
Objective—To evaluate the cardiopulmonary effects of anesthetic induction with thiopental, propofol, or ketamine hydrochloride and diazepam in dogs sedated with medetomidine and hydromorphone.
Animals—6 healthy adult dogs.
Procedures—Dogs received 3 induction regimens in a randomized crossover study. Twenty minutes after sedation with medetomidine (10 μg/kg, IV) and hydromorphone (0.05 mg/kg, IV), anesthesia was induced with ketamine-diazepam, propofol, or thiopental and then maintained with isoflurane in oxygen. Measurements were obtained prior to sedation (baseline), 10 minutes after administration of preanesthetic medications, after induction before receiving oxygen, and after the start of isoflurane-oxygen administration.
Results—Doses required for induction were 1.25 mg of ketamine/kg with 0.0625 mg of diazepam/kg, 1 mg of propofol/kg, and 2.5 mg of thiopental/kg. After administration of preanesthetic medications, heart rate (HR), cardiac index, and PaO2 values were significantly lower and mean arterial blood pressure, central venous pressure, and PaCO2 values were significantly higher than baseline values for all regimens. After induction of anesthesia, compared with postsedation values, HR was greater for ketamine-diazepam and thiopental regimens, whereas PaCO2 tension was greater and stroke index values were lower for all regimens. After induction, PaO2 values were significantly lower and HR and cardiac index values significantly higher for the ketamine-diazepam regimen, compared with values for the propofol and thiopental regimens.
Conclusions and Clinical Relevance—Medetomidine and hydromorphone caused dramatic hemodynamic alterations, and at the doses used, the 3 induction regimens did not induce important additional cardiovascular alterations. However, administration of supplemental oxygen is recommended.