OBJECTIVE To evaluate the use of a modified passive leg-raising maneuver (PLRM) to predict fluid responsiveness during experimental induction and correction of hypovolemia in isoflurane-anesthetized pigs.
ANIMALS 6 healthy male Landrace pigs.
PROCEDURES Pigs were anesthetized with isoflurane, positioned in dorsal recumbency, and instrumented. Following induction of a neuromuscular blockade, pigs were mechanically ventilated throughout 5 sequential experimental stages during which the blood volume was manipulated so that subjects transitioned from normovolemia (baseline) to hypovolemia (blood volume depletion, 20% and 40%), back to normovolemia, and then to hypervolemia. During each stage, hemodynamic variables were measured before and 3 minutes after a PLRM and 1 minute after the pelvic limbs were returned to their original position. The PLRM consisted of raising the pelvic limbs and caudal portion of the abdomen to a 15° angle relative to the horizontal plane.
RESULTS Hemodynamic variables did not vary in response to the PLRM when pigs were normovolemic or hypervolemic. When pigs were hypovolemic, the PLRM resulted in a significant increase in cardiac output and decrease in plethysomographic variability index and pulse pressure variation. When the pelvic limbs were returned to their original position, cardiac output and pulse pressure variation rapidly returned to their pre-PLRM values, but the plethysomographic variability index did not.
CONCLUSIONS AND CLINICAL RELEVANCE Results suggested a modified PLRM might be useful for identification of hemodynamically unstable animals that are likely to respond to fluid therapy. Further research is necessary to validate the described PLRM for prediction of fluid responsiveness in clinically ill animals.
OBJECTIVE To assess the isoflurane-sparing effect of a transdermal formulation of fentanyl solution (TFS) and subsequent naloxone administration in dogs.
ANIMALS 6 healthy mixed-breed dogs.
PROCEDURES Minimum alveolar concentration (MAC) of isoflurane was determined in each dog with a tail clamp method (baseline). Two weeks later, dogs were treated with TFS (2.7 mg/kg [1.23 mg/lb]), and the MAC of isoflurane was determined 4 and 24 hours later. After the 4-hour MAC assessment, saline (0.9% NaCl) solution was immediately administered IV and MAC was reassessed. After the 24-hour MAC assessment, naloxone hydrochloride (0.02 mg/kg [0.01 mg/lb], IV) was immediately administered and MAC was reassessed. Heart rate, respiratory rate, arterial blood pressure, end-tidal partial pressure of CO2, and oxygen saturation as measured by pulse oximetry were recorded for each MAC assessment.
RESULTS Mean ± SD MAC of isoflurane at 4 and 24 hours after TFS application was 45.4 ± 4.0% and 45.5 ± 4.5% lower than at baseline, respectively. Following naloxone administration, only a minimal reduction in MAC was identified (mean percentage decrease from baseline of 13.1 ± 2.2%, compared with 43.8 ± 5.6% for saline solution). Mean heart rate was significantly higher after naloxone administration (113.2 ± 22.2 beats/min) than after saline solution administration (76.7 ± 20.0 beats/min). No significant differences in other variables were identified among treatments.
CONCLUSIONS AND CLINICAL RELEVANCE The isoflurane-sparing effects of TFS in healthy dogs were consistent and sustained between 4 and 24 hours after application, and these effects should be taken into consideration when anesthetizing or reanesthetizing TFS-treated dogs.
Objective—To investigate hemodynamic effects of acepromazine and dexmedetomidine premedication in dogs undergoing general anesthesia induced with propofol and maintained with isoflurane in oxygen and assess the influence of these drugs on oxygen-carrying capacity and PCV.
Design—Prospective, randomized crossover study.
Animals—6 healthy adult dogs.
Procedures—Dogs received acepromazine (0.05 mg/kg [0.023 mg/lb]) or dexmedetomidine (15.0 μg/kg [6.82 μg/lb]) IM. Fifteen minutes later, anesthesia was induced with propofol and maintained at end-tidal isoflurane concentration of 1.28% (1 minimum alveolar concentration) for 30 minutes. Hemodynamic variables were recorded at predetermined times. The experiment was repeated 48 hours later with the alternate premedication. Results were analyzed by repeated-measures ANOVA with a mixed-models procedure.
Results—Bradycardia, hypertension, and significant cardiac output (CO) reduction developed after dexmedetomidine premedication but improved during isoflurane anesthesia. Hypotension developed after acepromazine administration and persisted throughout the isoflurane maintenance period, but CO was maintained throughout the anesthetic period when dogs received this treatment. Oxygen delivery and consumption were not different between treatments at most time points, whereas arterial oxygen content was lower with acepromazine premedication owing to lower PCV during isoflurane anesthesia.
Conclusions and Clinical Relevance—Acepromazine exacerbated hypotension, but CO did not change in dogs anesthetized with propofol and isoflurane. Dexmedetomidine reduced CO but prevented propofol-isoflurane–induced hypotension. In general, oxygen-carrying capacity and PCV were higher in dexmedetomidine-treated than in acepromazine-treated dogs anesthetized with propofol and isoflurane.
To evaluate cardiac output (CO) measurements using transpulmonary ultrasound (TPUD) technology and compare results with those of the gold standard, pulmonary arterial catheter thermodilution (PACTD), in 6 healthy anesthetized pigs during acute hemodynamic changes caused by manipulation of the blood volume.
6 healthy male Landrace pigs.
Over a period of 1 week, pigs were anesthetized with isoflurane, mechanically ventilated, and underwent instrumentation in dorsal recumbency. They were subjected to sequential experimental states during which the blood volume was manipulated so that the animals transitioned from normovolemia to hypovolemia (20% and 40% of blood volume depletion), back to normovolemia (autologous blood transfusion), and then to hypervolemia (following colloid bolus). During each volume state, CO measurements were compared between TPUD and PACTD.
The mean ± SD relative bias between TPUD and PACTD was 7.71% ± 21.2% with limits of agreement –33.9% to 49.3%, indicating TPUD slightly underestimated CO values, compared with values obtained with PACTD. The mean ± SD of the bias between the 2 methods was 0.13 ± 0.5 L/min. Only 5 of 36 (13.9%) TPUD CO measurements had an absolute value of relative bias > 30%. The percentage error calculated for TPUD was 29.4%.
Results suggested that TPUD measurements have acceptable agreement with PACTD measurements. Moreover, TPUD exhibits promising potential in being used interchangeably with PACTD for future hemodynamic research involving swine as species of interest.