Objective—To determine the cardiovascular effects of dopamine and dobutamine infusions during nor-movolemia, hypovolemia (HV) through blood loss of 10 mL/kg (HV10), further loss to 25 mL/kg (HV25), and volume replacement (VR) in isoflurane-anesthetized dogs.
Animals—7 healthy young dogs.
Procedures—Dogs were anesthetized with isoflurane 2 times (3 weeks apart). Cardiovascular measurements were obtained for each volume state. The cardiac index (CI) determined by the lithium dilution technique was compared with CI assessed by the arterial pulse contour technique. At each volume state, random treatment with dobutamine or dopamine was assessed (CI by the arterial pulse contour technique). Ten-minute treatments with 3 and6 μg of dobutamine/kg/min or 7 and 14 μg of dopamine/kg/min (low and high doses, respectively) were administered sequentially. Differences from baseline were determined for volume, drug, and dose effects.
Results—Significant proportional changes in blood pressure (BP), stroke index (SI), and CI were evident with changes in volume state. Systemic vascular resistance (SVR) decreased after VR. Dobutamine induced little change in BP; increased heart rate (HR), SI, and CI; and decreased SVR (high dose). Dopamine increased BP and SI, did not change CI, and increased SVR (high dose). The arterial pulse contour technique underestimated changes in CI associated with volume changes.
Conclusions and Clinical Relevance—Isoflurane eliminates clinically obvious compensatory increases in HR during HV. Dopamine is suitable for temporary management of blood loss in isoflurane-anesthetized dogs. Dobutamine increased CI without an associated improvement in BP. The arterial pulse contour monitor should be recalibrated when volume status changes.
Objective—To compare induction with hydromorphone
and diazepam (HydroD) or oxymorphone and
diazepam (OxyD) followed by maintenance with
isoflurane in dogs with induced hypovolemia.
Animals—6 healthy mixed-breed dogs.
Procedure—The study used a crossover design.
Measurements were obtained in normovolemic dogs
during isoflurane. Hypovolemia was induced (blood
loss of 30 mL/kg) and measurements repeated following
recovery from anesthesia, after HydroD
(hydromorphone, 0.1 mg/kg; diazepam, 0.2 mg/kg; IV)
or OxyD (oxymorphone, 0.05 mg/kg; diazepam,
0.2 mg/kg; IV), after another dose of the same opioid,
during administration of isoflurane (end-tidal concentration,
0.9%), and after glycopyrrolate (0.01 mg/kg,
IV). Significant changes were identified.
Results—Induction effect was evident within 1 minute.
All dogs were intubated after the second dose of opioid.
No significant differences were found between inductions.
The HydroD decreased heart rate (mean ± SEM,
–41 ± 9.8 beats/min), whereas both inductions
increased stroke index (0.4 ± 0.09 mL/kg/beat) and
caused moderate respiratory depression. Cardiac index
was decreased (±30.2 ± 6.04 mL/kg/min) and there was
minor metabolic acidosis during isoflurane following
HydroD, compared with values for anesthetized normovolemic
dogs. Glycopyrrolate increased heart rate (50 ±
8.6 beats/min) and decreased systolic blood pressure
(–23.2 ± 4.87 mm Hg) in dogs induced with HydroD and
decreased stroke index (–0.3 ± 0.08 mL/kg/beat) for both
Conclusions and Clinical Relevance—Similar effects
were detected after administration of HydroD or OxyD
in hypovolemic dogs. Either combination should be
safe for use in hypovolemic dogs. Administration of
glycopyrrolate was not beneficial. (Am J Vet Res
Objective—To determine whether administration of
the nonsteroidal anti-inflammatory drugs meloxicam
or carprofen to healthy dogs that were subsequently
anesthetized and subjected to painful electrical stimulation
has adverse effects on renal function as measured
by glomerular filtration rate (GFR) and evaluation
of serum concentrations of urea and creatinine.
Animals—6 male and 6 female healthy young-adult
Procedure—A study was conducted in accordance
with a randomized crossover Latin-square design.
One of 3 treatments (saline [0.9% NaCl] solution,
0.2 mg of meloxicam/kg, or 4.0 mg of carprofen/kg)
was administered IV 1 hour before anesthesia was
induced by use of drugs in accordance with a standard
anesthetic protocol (butorphanol tartrate and
acepromazine maleate as preanesthetic medications,
ketamine hydrochloride and diazepam for induction,
and maintenance with isoflurane). Anesthetized dogs
were subjected to intermittent electrical stimulation
for 30 minutes. Direct, mean arterial blood pressure;
heart rate; and respiratory rate were monitored. End-tidal
isoflurane concentration was maintained at 1.5
times the minimum alveolar concentration. The GFR,
as measured by plasma clearance of 99mTc-diethylenetriaminepentaacetic
acid, and serum concentrations of serum and creatinine were determined 24
hours after induction of anesthesia.
Results—Neither meloxicam nor carprofen significantly
affected GFR or serum concentrations of urea
and creatinine, compared with values for the saline
Conclusions and Clinical Relevance—When administered
1 hour before onset of anesthesia and painful
electrical stimulation, meloxicam or carprofen did not
cause clinically important alterations of renal function in
young healthy dogs. (Am J Vet Res 2004;65:1384–1390)
Objective—To evaluate the dose-related cardiovascular and urine output (UrO) effects of dopamine hydrochloride and dobutamine hydrochloride, administered individually and in combination at various ratios, and identify individual doses that achieve target mean arterial blood pressure (MAP; 70 mm Hg) and cardiac index (CI; 150 mL/kg/min) in dogs during deep isoflurane anesthesia.
Animals—10 young clinically normal dogs.
Procedures—Following isoflurane equilibration at a baseline MAP of 50 mm Hg on 3 occasions, dogs randomly received IV administration of dopamine (3, 7, 10, 15, and 20 μg/kg/min), dobutamine (1, 2, 4, 6, and 8 μg/kg/min), and dopamine-dobutamine combinations (3.5:1, 3.5:4, 7:2, 14:1, and 14:4 μg/kg/min) in a crossover study. Selected cardiovascular and UrO effects were determined following 20-minute infusions at each dose.
Results—Dopamine caused significant dose-dependent responses and achieved target MAP and CI at 7 μg/kg/min; dobutamine at 2 μg/kg/min significantly affected only CI values. At any dose, dopamine significantly affected UrO, whereas dobutamine did not. Target MAP and CI values were achieved with a dopamine-dobutamine combination at 7:2 μg/kg/min; a dopamine-related dose response for MAP and dopamine- and dobutamine-related dose responses for CI were identified. Changes in UrO were associated with dopamine only.
Conclusions and Clinical Relevance—In isoflurane-anesthetized dogs, a guideline dose for dopamine of 7 μg/kg/min is suggested; dobutamine alone did not improve MAP. Data regarding cardiovascular and UrO effects indicated that the combination of dopamine and dobutamine did not provide greater benefit than use of dopamine alone in dogs.
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.
Objective—To assess agreement between arterial
pressure waveform–derived cardiac output (PCO) and
lithium dilution cardiac output (LiDCO) systems in
measurements of various levels of cardiac output
(CO) induced by changes in anesthetic depth and
administration of inotropic drugs in dogs.
Animals—6 healthy dogs.
Procedure—Dogs were anesthetized on 2 occasions
separated by at least 5 days. Inotropic drug administration
(dopamine or dobutamine) was randomly
assigned in a crossover manner. Following initial calibration
of PCO measurements with a LiDCO measurement,
4 randomly assigned treatments were
administered to vary CO; subsequently, concurrent
pairs of PCO and LiDCO measurements were
obtained. Treatments included a light plane of anesthesia,
deep plane of anesthesia, continuous infusion
of an inotropic drug (rate adjusted to achieve a mean
arterial pressure of 65 to 80 mm Hg), and continuous
infusion of an inotropic drug (7 µg/kg/min).
Results—Significant differences in PCO and LiDCO
measurements were found during deep planes of
anesthesia and with dopamine infusions but not during
the light plane of anesthesia or with dobutamine
infusions. The PCO system provided higher CO measurements
than the LiDCO system during deep
planes of anesthesia but lower CO measurements
during dopamine infusions.
Conclusions and Clinical Relevance—The PCO system
tracked changes in CO in a similar direction as
the LiDCO system. The PCO system provided better
agreement with LiDCO measurements over time
when hemodynamic conditions were similar to those
during initial calibration. Recalibration of the PCO system
is recommended when hemodynamic conditions
or pressure waveforms are altered appreciably. (Am J Vet Res 2005;66:1430–1436)
Objective—To determine the minimum alveolar concentration
(MAC) of sevoflurane and assess the
sevoflurane-sparing effect of coadministration of
nitrous oxide in mechanically ventilated Dumeril monitors
Design—Prospective crossover study.
Animals—10 healthy adult Dumeril monitors.
Procedure—Anesthesia was induced with sevoflurane
in 100% oxygen or sevoflurane in 66% nitrous
oxide (N2O) with 34% oxygen, delivered through a
face mask. Monitors were endotracheally intubated,
and end-tidal and inspired isoflurane concentrations
were measured continuously; MAC was determined
by use of a standard bracketing technique. An electrical
stimulus (50 Hz, 50 V) was delivered to the ventral
aspect of the tail as the supramaximal stimulus. A
blood sample for blood gas analyses was collected
from the ventral coccygeal vessels at the beginning
and end of the anesthetic period. An interval of at least
7 days was allowed to elapse between treatments.
Results—The MAC ± SDs of sevoflurane in oxygen and
with N2O were 2.51 ± 0.46% and 1.83 ± 0.33%, respectively.
There was a significant difference between the 2
treatments, and the mean MAC-reducing effect of N2O
was 26.4 ± 11.4%. Assuming simple linear additivity of
sevoflurane and N2O, the MAC for N2O was estimated
to be 244%. No significant differences in blood gas values—with the predictable exception of oxygen pressure—were detected between the 2 groups.
Conclusions and Clinical Relevance—The MAC of
sevoflurane in Dumeril monitors is similar to that
reported for other species. The addition of N2O significantly
decreased the MAC of sevoflurane in this
species. (J Am Vet Med Assoc 2005;227:575–578)