Objective—To evaluate the effect of dilution of blood
samples with sodium heparin on blood gas, electrolyte,
and lactate measurements in dogs.
Sample Population—Venous blood samples collected
from 6 adult dogs of various breeds.
Procedure—Syringes were prepared with anticoagulant
via 1 of 4 techniques, and the residual volume of
liquid heparin in each type of prepared syringe was
determined. Blood gas values and other selected clinicopathologic
variables were measured in whole
blood samples after collection (baseline) and after
aliquots of the samples were diluted with heparin via
1 of the 4 manual syringe techniques. By use of a
tonometer, whole blood samples were adjusted to 1
of 3 oxygen concentrations (40, 100, or 600 mm Hg)
and the PO2 values were measured at baseline and
subsequent to the 4 heparin dilutions.
Results—The 4 syringe techniques resulted in 3.9%,
9.4%, 18.8%, and 34.1% dilutions of a 1-mL blood
sample. Compared with baseline values, dilution of
blood samples with liquid heparin significantly
changed the measured values of PCO2, PO2, and base
deficit and concentrations of electrolytes and lactate.
Of the variables assessed, measurement of ionized
calcium concentration in blood was most affected by
Conclusions and Clinical Relevance—These findings
in dogs indicate that dilution of blood samples
with heparin can be a source of preanalytical error in
blood gas, electrolyte, and lactate measurements.
Limiting dilution of blood samples with heparin to
< 4% by volume via an evacuation technique of
syringe heparinization is recommended. (Am J Vet Res 2005;66:656–660)
Objective—To evaluate the use of a transesophageal echo-Doppler ultrasonography (TED) technique for measurement of aortic blood flow (ABF) in relation to cardiac output (CO) measured by use of a thermodilution technique in anesthetized cats.
Procedures—Anesthesia was induced and maintained in cats by administration of isoflurane. A thermodilution catheter was placed in a pulmonary artery. The TED probe was positioned in the esophagus in the region where the aorta and esophagus are almost parallel. Five baseline values for ABF and CO were concurrently recorded. Cats were randomly assigned to a high or low CO state (increase or decrease in CO by at least 25% from baseline, respectively). Baseline conditions were restored, and the other CO state was induced, after which baseline conditions were again restored. For each CO state, ABF and CO were measured 5 times at 5-minute intervals. Correlation and agreement between the techniques were determined by use of the Pearson product-moment correlation and Bland-Altman method.
Results—CO ranged from 0.16 to 0.75 L/min and ABF from 0.05 to 0.48 L/min. Overall data analysis revealed a high correlation (r = 0.884) between techniques but poor agreement (limits of agreement, −0.277 to 0.028 L/min). During the low CO state, correlation between techniques was low (r = 0.413).
Conclusions and Clinical Relevance—TED did not accurately measure CO. However, it allowed evaluation of CO patterns and may be useful clinically in anesthetized cats.
Objective—To evaluate the analgesic efficacy of ABT-116, a transient receptor potential cation channel vanilloid subfamily V member 1 antagonist, and compare it with that of buprenorphine by measurement of mechanical and thermal nociceptive thresholds in dogs.
Animals—Six 7- to 8-month-old dogs (3 males and 3 females).
Procedures—In a crossover study design, all dogs received ABT-116 (30 mg/kg, PO) and buprenorphine (0.03 mg/kg, orotransmucosally), with each treatment separated by 1 week. Physiologic variables were recorded prior to and 1, 6, and 24 hours after drug administration. Thermal (thoracic) and mechanical (dorsolateral aspect of the radius [proximal] and dorsopalmar aspect of the forefoot [distal]) nociceptive thresholds were assessed prior to (baseline) and 15 minutes and 1, 2, 4, 6, 12, 18, and 24 hours after treatment.
Results—Buprenorphine administration resulted in higher overall thermal and proximal mechanical nociceptive thresholds, compared with ABT-116. Distal mechanical nociceptive thresholds after treatment were higher than baseline values for both treatments, but the magnitude of change was greater for buprenorphine at 1 hour after administration. Whereas HR and RR sporadically differed from baseline values after ABT-116 administration, rectal temperature increased from a baseline value of 39 ± 0.2°C (mean ± SD) to a peak of 40.6 ± 0.2°C at 6 hours.
Conclusions and Clinical Relevance—In dogs without inflammation or nerve injury, PO administration of ABT-116 did not consistently result in an increase in nociceptive thresholds. However, clinically relevant increases in rectal temperature were identified after ABT-116 administration.
Objective—To determine plasma concentrations and behavioral, antinociceptive, and physiologic effects of methadone administered via IV and oral transmucosal (OTM) routes in cats.
Animals—8 healthy adult cats.
Procedures—Methadone was administered via IV (0.3 mg/kg) and OTM (0.6 mg/kg) routes to each cat in a balanced crossover design. On the days of drug administration, jugular catheters were placed in all cats under anesthesia; a cephalic catheter was also placed in cats that received methadone IV. Baseline measurements were obtained ≥ 90 minutes after extubation, and methadone was administered via the predetermined route. Heart and respiratory rates were measured; sedation, behavior, and antinociception were evaluated, and blood samples were collected for methadone concentration analysis at predetermined intervals for 24 hours after methadone administration. Data were summarized and evaluated statistically.
Results—Plasma concentrations of methadone were detected rapidly after administration via either route. Peak concentration was detected 2 hours after OTM administration and 10 minutes after IV administration. Mean ± SD peak concentration was lower after OTM administration (81.2 ± 14.5 ng/mL) than after IV administration (112.9 ± 28.5 ng/mL). Sedation was greater and lasted longer after OTM administration. Antinociceptive effects were detected 10 minutes after administration in both groups; these persisted ≥ 2 hours after IV administration and ≥ 4 hours after OTM administration.
Conclusions and Clinical Relevance—Despite lower mean peak plasma concentrations, duration of antinociceptive effects of methadone was longer after OTM administration than after IV administration. Methadone administered via either route may be useful for perioperative pain management in cats.
Objective—To compare cardiovascular effects of sevoflurane alone and sevoflurane plus an IV infusion of lidocaine in horses.
Animals—8 adult horses.
Procedures—Each horse was anesthetized twice via IV administration of xylazine, diazepam, and ketamine. During 1 anesthetic episode, anesthesia was maintained by administration of sevoflurane in oxygen at 1.0 and 1.5 times the minimum alveolar concentration (MAC). During the other episode, anesthesia was maintained at the same MAC multiples via a reduced concentration of sevoflurane plus an IV infusion of lidocaine. Heart rate, arterial blood pressures, blood gas analyses, and cardiac output were measured during mechanical (controlled) ventilation at both 1.0 and 1.5 MAC for each anesthetic protocol and during spontaneous ventilation at 1 of the 2 MAC multiples.
Results—Cardiorespiratory variables did not differ significantly between anesthetic protocols. Blood pressures were highest at 1.0 MAC during spontaneous ventilation and lowest at 1.5 MAC during controlled ventilation for either anesthetic protocol. Cardiac output was significantly higher during 1.0 MAC than during 1.5 MAC for sevoflurane plus lidocaine but was not affected by anesthetic protocol or mode of ventilation. Clinically important hypotension was detected at 1.5 MAC for both anesthetic protocols.
Conclusions and Clinical Relevance—Lidocaine infusion did not alter cardiorespiratory variables during anesthesia in horses, provided anesthetic depth was maintained constant. The IV administration of lidocaine to anesthetized nonstimulated horses should be used for reasons other than to improve cardiovascular performance. Severe hypotension can be expected in nonstimulated horses at 1.5 MAC sevoflurane, regardless of whether lidocaine is administered.
Objective—To determine effects of a continuous rate infusion of lidocaine on the minimum alveolar concentration (MAC) of sevoflurane in horses.
Animals—8 healthy adult horses.
Procedures—Horses were anesthetized via IV administration of xylazine, ketamine, and diazepam; anesthesia was maintained with sevoflurane in oxygen. Approximately 1 hour after induction, sevoflurane MAC determination was initiated via standard techniques. Following sevoflurane MAC determination, lidocaine was administered as a bolus (1.3 mg/kg, IV, over 15 minutes), followed by constant rate infusion at 50 μg/kg/min. Determination of MAC for the lidocaine-sevoflurane combination was started 30 minutes after lidocaine infusion was initiated. Arterial blood samples were collected after the lidocaine bolus, at 30-minute intervals, and at the end of the infusion for measurement of plasma lidocaine concentrations.
Results—IV administration of lidocaine decreased mean ± SD sevoflurane MAC from 2.42 ± 0.24% to 1.78 ± 0.38% (mean MAC reduction, 26.7 ± 12%). Plasma lidocaine concentrations were 2,589 ± 811 ng/mL at the end of the bolus; 2,065 ± 441 ng/mL, 2,243 ± 699 ng/mL, 2,168 ± 339 ng/mL, and 2,254 ± 215 ng/mL at 30, 60, 90, and 120 minutes of infusion, respectively; and 2,206 ± 329 ng/mL at the end of the infusion. Plasma concentrations did not differ significantly among time points.
Conclusions and Clinical Relevance—Lidocaine could be useful for providing a more balanced anesthetic technique in horses. A detailed cardiovascular study on the effects of IV infusion of lidocaine during anesthesia with sevoflurane is required before this combination can be recommended.
Objective—To determine outcome of positive-pressure ventilation (PPV) for 24 hours or longer and identify factors associated with successful weaning from PPV and survival to hospital discharge in dogs and cats.
Design—Retrospective case series.
Animals—124 dogs and 24 cats that received PPV for 24 hours or longer.
Procedures—Medical records were reviewed for signalment, primary diagnosis, reason for initiating PPV, measures of oxygenation and ventilation before and during PPV, ventilator settings, complications, duration of PPV, and outcome. Animals were categorized into 1 of 3 groups on the basis of the reason for PPV.
Results—Group 1 patients received PPV for inadequate oxygenation (67 dogs and 6 cats), group 2 for inadequate ventilation (46 dogs and 16 cats), and group 3 for inadequate oxygenation and ventilation (11 dogs and 2 cats). Of the group 1 animals, 36% (26/73) were weaned from PPV and 22% (16/73) survived to hospital discharge. In group 2, 50% (31/62) were weaned from PPV and 39% (24/62) survived to hospital discharge. In group 3, 3 of 13 were weaned from PPV and 1 of 13 survived to hospital discharge. Likelihood of successful weaning and survival to hospital discharge were significantly higher for group 2 animals, and cats had a significantly lower likelihood of successful weaning from PPV, compared with dogs. Median duration of PPV was 48 hours (range, 24 to 356 hours) and was not as-sociated with outcome.
Conclusions and Clinical Relevance—Results suggested that long-term PPV is practical and successful in dogs and cats.
To evaluate the sedative and cardiopulmonary effects of various combinations of acepromazine, dexmedetomidine, hydromorphone, and glycopyrrolate, followed by anesthetic induction with propofol and maintenance with isoflurane in healthy dogs.
6 healthy adult female Beagles.
Dogs were instrumented for hemodynamic measurements while anesthetized with isoflurane. Two hours after recovery, dogs received 1 of 4 IM combinations in a crossover design with 1 week between treatments: hydromorphone (0.1 mg/kg) and acepromazine (0.005 mg/kg; HA); hydromorphone and dexmedetomidine (0.0025 mg/kg; HD); hydromorphone, acepromazine, and dexmedetomidine (HAD); and hydromorphone, acepromazine, dexmedetomidine, and glycopyrrolate (0.02 mg/kg; HADG). Sedation was scored after 30 minutes. Physiologic variables and cardiac index were measured after sedation, after anesthetic induction with propofol, and every 15 minutes during maintenance of anesthesia with isoflurane for 60 minutes (target expired concentration at 760 mm Hg, 1.3%).
Sedation scores were not significantly different among treatments. Mean ± SD cardiac index was significantly higher for the HA (202 ± 45 mL/min/kg) and HADG (185 ± 59 mL/min/kg) treatments than for the HD (88 ± 31 mL/min/kg) and HAD (103 ± 25 mL/min/kg) treatments after sedation and through the first 15 minutes of isoflurane anesthesia. No ventricular arrhythmias were noted with any treatment.
In healthy dogs, IM administration of HADG before propofol and isoflurane anesthesia provided acceptable cardiopulmonary function with no adverse effects. This combination should be considered for routine anesthetic premedication in healthy dogs.