The impact of acepromazine on the efficacy of crystalloid, dextran or ephedrine treatment in hypotensive dogs under isoflurane anesthesia.

OBJECTIVE: To determine the impact of acepromazine on the cardiovascular responses to three treatments for hypotension in dogs during deep isoflurane anesthesia. STUDY DESIGN: Prospective blinded randomized cross-over experimental design. ANIMALS: Six adult (2.5 ± 0.5 year old) healthy mixed breed dogs (24.2 ± 7.6 kg). METHODS: Anesthesia was induced with propofol (4-6 mg kg(-1) , IV) and maintained with isoflurane. Each dog received six treatments separated by at least 5 days. Once instrumented, dogs randomly received acepromazine (0.05 mg kg(-1) ) (Ace) or saline (equal volume) (Sal) IV and end-tidal isoflurane (E'Iso) was adjusted to achieve hypotension, defined as a mean blood pressure between 45 and 50 mmHg. Dogs randomly received dextran (D) (7 mL kg(-1) ) or lactated Ringer's (LR) (20 mL kg(-1) ) over 14 minutes, or ephedrine (Eph) (0.1 mg kg(-1) followed by 10 µg kg(-1) minute(-1) ) throughout the study. Measurements were taken at baseline, 5, 10, 15, 20, 30, and 40 minutes. Data were analyzed with a Latin Square in two factors (Ace/Sal and treatment) for repeated measures, with further comparisons if appropriate (p < 0.05). RESULTS: E'Iso producing hypotension was significantly less following Ace (2.07 ± 0.23%) than Sal (2.43 ± 0.23%). No improvement in cardiac output (CO) was observed with D or LR. LR initially intensified hypotension with a significant reduction in SVR, while D caused a minor improvement in ABP. Eph produced a significant increase in ABP, CO, hemoglobin, oxygen content and delivery. Pre-treatment with Ace minimized ABP improvements with all treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Acepromazine (0.05 mg kg(-1) IV) enhanced the hypotensive effect of isoflurane, although it maintained CO. Administration of LR significantly worsens ABP initially by further vasodilation. D caused minimal improvement in ABP. At the infusion studied, Eph effectively countered the cardiovascular depression produced by deep isoflurane anesthesia, but extremes in ABP associated with initial vasoconstriction prevent our recommendation at this dose.

Positive pressure ventilation during anesthesia in dogs: Assessment of surface area derived tidal volume.

The purpose of this study was to assess the use of surface area derived tidal volume in anesthetized ventilated dogs (n = 71, random assignment) compared to settings by experienced personnel. There was no significant difference (P = 0.1030) between methods (p(a)CO(2) of 43.1 ± 7 mmHg and 39.8 ± 7 mmHg, respectively). Surface area derived tidal volume can achieve satisfactory ventilation.

The cardiopulmonary effects of anesthetic induction with isoflurane, ketamine-diazepam or propofol-diazepam in the hypovolemic dog.

OBJECTIVE: To evaluate and compare the cardiopulmonary effects of induction of anesthesia with isoflurane (Iso), ketamine-diazepam (KD), or propofol-diazepam (PD) in hypovolemic dogs. Study design Prospective randomized cross-over trial. ANIMALS: Six healthy intact, mixed breed, female dogs weighing 20.7 +/- 4.2 kg and aged 22 +/- 2 months. Methods Dogs had 30 mL kg(-1) of blood removed at a rate of 1.5 mL kg(-1) minute(-1) under isoflurane anesthesia. Following a 30-minute recovery period, anesthesia was reinduced. Dogs were assigned to one of three treatments: isoflurane via facemask using 0.5% incremental increases in the delivered concentration every 30 seconds, 1.25 mg kg(-1) ketamine and 0.0625 mg kg(-1) diazepam intravenously (IV) with doses repeated every 30 seconds as required, and 2 mg kg(-1) propofol and 0.2 mg kg(-1) diazepam IV followed by 1 mg kg(-1) propofol increments IV every 30 seconds as required. Following endotracheal intubation all dogs received 1.7% end-tidal isoflurane in oxygen. Cardiopulmonary variables were recorded at baseline (before induction) and at 5 or 10 minute intervals following endotracheal intubation. RESULTS: Induction time was longer in Iso (4.98 +/- 0.47 minutes) compared to KD (3.10 +/- 0.47 minutes) or PD (3.22 +/- 0.45 minutes). To produce anesthesia, KD received 4.9 +/- 2.3 mg kg(-1) ketamine and 0.24 +/- 0.1 mg kg(-1) diazepam, while PD received 2.2 +/- 0.4 mg kg(-1) propofol and 0.2 mg kg(-1) diazepam. End-tidal isoflurane concentration immediately following intubation was 1.7 +/- 0.4% in Iso. Arterial blood pressure and heart rate were significantly higher in KD and PD compared to Iso and in KD compared to PD. Arterial carbon dioxide partial pressure was significantly higher in PD compared to KD and Iso immediately after induction. CONCLUSIONS AND CLINICAL RELEVANCE: In hypovolemic dogs, KD or PD, as used in this study to induce anesthesia, resulted in less hemodynamic depression compared to isoflurane.

Cardiopulmonary effects of anesthetic induction with thiopental, propofol, or a combination of ketamine hydrochloride and diazepam in dogs sedated with a combination of medetomidine and hydromorphone.

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 microg/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 PaO(2) values were significantly lower and mean arterial blood pressure, central venous pressure, and PaCO(2) 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 PaCO(2) tension was greater and stroke index values were lower for all regimens. After induction, PaO(2) 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.

Perioperative pain management in veterinary patients.

Pain exists; however, we can prevent it, and we can treat it. The fallacy that pain is protective and must be allowed to avoid risk for damage after surgery needs to be eradicated. Preoperative and postoperative analgesia is directed at aching pain, whereas sharp pain associated with inappropriate movements persists. Analgesia provides much more benefit than concern. This article provides suggestions for development of an analgesic plan from the point of admission to discharge. These guidelines can then be adjusted according to the patient's needs and responses.

Analgesia and chemical restraint for the emergent veterinary patient.

Frequently, analgesics are withheld in the emergent patient based on common misconceptions. Concerns expressed are that analgesics "mask" physiologic indicators of patient deterioration or that potential toxicity and adverse reactions associated with drug administration outweigh the benefits gained. Appropriate selection of drugs and doses as described in this article allow the veterinarian to achieve analgesia, in addition to sedation or restraint when needed, without unwarranted fears. Guidelines are provided for typical situations encountered in trauma patients to provide a safe starting point for providing analgesia. Caution required in these cases is also discussed, with emphasis on individualization of the approach to analgesia and chemical restraint.

Response of hypotensive dogs to dopamine hydrochloride and dobutamine hydrochloride during deep isoflurane anesthesia.

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 microg/kg/min), dobutamine (1, 2, 4, 6, and 8 microg/kg/min), and dopamine-dobutamine combinations (3.5:1, 3.5:4, 7:2, 14:1, and 14:4 microg/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 microg/kg/min; dobutamine at 2 microg/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 microg/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 microg/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.

Impact of dopamine or dobutamine infusions on cardiovascular variables after rapid blood loss and volume replacement during isoflurane-induced anesthesia in dogs.

OBJECTIVE: To determine the cardiovascular effects of dopamine and dobutamine infusions during nor-movolemia, hypovolemia (HV) through blood loss of 10 mL/kg (HV(10)), further loss to 25 mL/kg (HV(25)), 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 and 6 microg of dobutamine/kg/min or 7 and 14 microg 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.

Delay in final publication following abstract presentation: American College of Veterinary Anesthesiologists annual meeting.

RATIONALE FOR THE STUDY: A review of abstracts presented at nine annual meetings of the American College of Veterinary Anesthesiologists was undertaken to determine the average time to publication and the differences found between conference abstracts and final publications. Concerns about and advantages of using such abstracts in our teaching are considered. METHODOLOGY: Conference proceedings during the years 1990 through 1999 were considered. Key word and author searches using two common search engines were carried out to find whether abstracts presented had been published. The original article or its abstract was reviewed for consistency with the conference abstract. RESULTS: Of 283 abstracts examined, 73.5% were published in journals as full articles. The overall delay (+/-SD) in publication was 24.3 +/- 21.0 months. Common reasons for not publishing included too little time, more interest in carrying out the work than in writing it up, and other more demanding tasks. Authors indicated the intention of completing a submission on approximately 10% of the unpublished abstracts. The final articles reviewed showed major differences in key aspects from the abstract presented in 7% of the cases. In half of these cases, clinical action could have been affected by a change in emphasis of the conclusions. CONCLUSIONS: Because of the delay in publication of research, peer review of standardized abstracts should be encouraged. This material can be used to introduce students to new drugs, techniques, and results that may not otherwise become available until after their graduation. However, caution must be exercised in using this information, both because significant differences were noted in final publications and because unpublished research may be poorly interpreted at the time of presentation. This study emphasizes the value of critical review and lifelong learning in our careers.

Evaluation of induction by use of a combination of oxymorphone and diazepam or hydromorphone and diazepam and maintenance of anesthesia by use of isoflurane in dogs with experimentally induced hypovolemia.

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; i.v.) or OxyD (oxymorphone, 0.05 mg/kg; diazepam, 0.2 mg/kg; i.v.), after another dose of the same opioid, during administration of isoflurane (end-tidal concentration, 0.9%), and after glycopyrrolate (0.01 mg/kg, i.v.). 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 inductions. 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.

Comparison of arterial pressure waveform analysis with the lithium dilution technique to monitor cardiac output in anesthetized dogs.

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 microg/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.

Anesthetic potency of sevoflurane with and without nitrous oxide in mechanically ventilated Dumeril monitors.

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 (Varanus dumerili). 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.

Analgesia and chemical restraint for the emergent patient.

This article discusses analgesia and chemical restraint for the emergency patient. As illness or injury affect all organ systems, specific recommendations and considerations of analgesic, anesthetic, and restraining regimens are presented. As animals of all ages, from neonates to geriatric and those that are pregnant or lactating,may require management of their illness or injury, recommendations for these patients are also presented.

Effect of meloxicam and carprofen on renal function when administered to healthy dogs prior to anesthesia and painful stimulation.

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 Beagles. 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 i.v. 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 treatment. 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.

Non-linear, visual-rich supplemental material designed for an introductory course in veterinary anesthesia.

A possible reason for superficial learning in an introductory anesthesia course was considered to be a lack of visual reinforcement at the time of examination preparation. Students had limited access to live animal laboratories and clinical cases during the course, reducing their ability to depend on experiential learning. In an attempt to improve student learning, simple presentation software was used to develop a supplemental CD. The design involved multiple PowerPoint presentations that incorporated text, pictures, videos, and self-assessments. Non-linear exploration of the topics covered was made possible by extensive use of hyperlinks within and between presentations, moving the student to definitions, background material, videos, advanced details, and previously covered information. Comments received from students on a prototype were positive overall, and improvements were made related to their feedback. Other supplemental materials and lecture presentations can easily incorporate the techniques described here.

Influence of prior determination of baseline minimum alveolar concentration (MAC) of isoflurane on the effect of ketamine on MAC in dogs.

The objective of this study was to determine if prior measurement of the minimum alveolar concentration (MAC) of isoflurane influences the effect of ketamine on the MAC of isoflurane in dogs. Eight mixed-breed dogs were studied on 2 occasions. Anesthesia was induced and maintained using isoflurane. In group 1 the effect of ketamine on isoflurane MAC was determined after initially finding the baseline isoflurane MAC. In group 2, the effect of ketamine on isoflurane MAC was determined without previous measure of the baseline isoflurane MAC. In both groups, MAC was determined again 30 min after stopping the CRI of ketamine. Plasma ketamine concentrations were measured during MAC determinations. In group 1, baseline MAC (mean ± SD: 1.18 ± 0.14%) was decreased by ketamine (0.88 ± 0.14%; P < 0.05). The MAC after stopping ketamine was similar (1.09 ± 0.16%) to baseline MAC and higher than with ketamine (P < 0.05). In group 2, the MAC with ketamine (0.79 ± 0.11%) was also increased after stopping ketamine (1.10 ± 0.17%; P < 0.05). The MAC values with ketamine were different between groups (P < 0.05). Ketamine plasma concentrations were similar between groups during the events of MAC determination. The MAC of isoflurane during the CRI of ketamine yielded different results when methods of same day (group-1) versus separate days (group-2) are used, despite similar plasma ketamine concentrations with both methods. However, because the magnitude of this difference was less than 10%, either method of determining MAC is deemed acceptable for research purposes.

L'objectif de la présente étude était de déterminer si une mesure antérieure de la concentration alvéolaire minimum (MAC) d'isoflurane influence l'effet de la kétamine sur la MAC d'isoflurane chez les chiens. Huit chiens de race croisée ont été examinés à deux occasions. L'anesthésie fut induite et maintenue à l'aide d'isoflurane. Dans le groupe 1, l'effet de la kétamine sur la MAC d'isoflurane fut déterminé après avoir initialement trouvé la MAC de base de l'isoflurane. Dans le groupe 2, l'effet de la kétamine sur la MAC d'isoflurane fut déterminé sans mesure préalable de la MAC de base de l'isoflurane. Dans les deux groupes la MAC fut déterminée de nouveau 30 min après l'arrêt de la CRI de kétamine. Les concentrations de kétamine plasmatiques furent mesurées durant les déterminations de MAC.Dans le groupe 1, la MAC de base (moyenne ± SD : 1,18 ± 0,14 %) fut diminuée par la kétamine (0,88 ± 0,14 %; P < 0,05). La MAC après l'arrêt de la kétamine était similaire (1,09 ± 0,16 %) à la MAC de base et plus élevée qu'avec la kétamine (P < 0,05). Dans le groupe 2, la MAC avec kétamine (0,79 ± 0,11 %) était également augmentée après l'arrêt de la kétamine (1,10 ± 0,17 %; P < 0,05). Les valeurs de MAC avec la kétamine étaient différentes entre les groupes (P < 0,05). Les concentrations plasmatiques de kétamine étaient similaires durant la détermination des MAC.La MAC d'isoflurane durant la CRI de kétamine a donné des résultats différents lorsque les méthodes d'un jour unique (le groupe 1) versus des jours séparés (le groupe 2) étaient utilisées, malgré des concentrations plasmatiques de kétamine similaires avec les deux méthodes. Toutefois, étant donné que l'ampleur de cette différence était de moins de 10 %, chacune des deux méthodes pour déterminer la MAC est considérée comme acceptable à des fins de recherche.(Traduit par Docteur Serge Messier).

Prior determination of baseline minimum alveolar concentration (MAC) of isoflurane does not influence the effect of ketamine on MAC in rabbits.

The objective of this study was to compare the effect on the minimum alveolar concentration (MAC) of isoflurane when ketamine was administered either after or without prior determination of the baseline MAC of isoflurane in rabbits. Using a prospective randomized crossover study, 8 adult, female New Zealand rabbits were allocated to 2 treatment groups. Anesthesia was induced and maintained with isoflurane. Group 1 (same-day determination) had the MAC-sparing effect of ketamine [1 mg/kg bodyweight (BW) bolus followed by a constant rate infusion (CRI) of 40 µg/kg BW per min, given by intravenous (IV)], which was determined after the baseline MAC of isoflurane was determined beforehand. A third MAC determination was started 30 min after stopping the CRI. Group 2 (separate-day determination) had the MAC-sparing effect of ketamine determined without previous determination of the baseline MAC of isoflurane. A second MAC determination was started 30 min after stopping the CRI. In group 1, the MAC of isoflurane (2.15 ± 0.09%) was significantly decreased by ketamine (1.63 ± 0.07%). After stopping the CRI, the MAC was significantly less (2.04 ± 0.11%) than the baseline MAC of isoflurane and significantly greater than the MAC during the CRI. In group 2, ketamine decreased isoflurane MAC (1.53 ± 0.22%) and the MAC increased significantly (1.94 ± 0.25%) after stopping the CRI. Minimum alveolar concentration (MAC) values did not differ significantly between the groups either during ketamine administration or after stopping ketamine. Under the study conditions, prior determination of the baseline isoflurane MAC did not alter the effect of ketamine on MAC. Both methods of determining MAC seemed to be valid for research purposes.

L'objectif de la présente étude était de comparer l'effet de la concentration alvéolaire minimale (MAC) d'isoflurane lorsque de la kétamine était administrée soit après ou sans détermination préalable de la MAC de base d'isoflurane chez les lapins. Au moyen d'une étude prospective aléatoire croisée, huit lapines adultes de race Nouvelle-Zélande ont été réparties dans deux groupes de traitement. Une anesthésie a été induite et maintenue avec de l'isoflurane. Le groupe 1 (détermination le même jour), a eu l'effet atténuant sur la MAC de la kétamine [bolus de 1 mg/kg de poids corporel (BW) suivi d'une infusion à taux constant (CRI) de 40 µg/kg BW par minute, administré par voie intraveineuse (IV)], déterminé après que la MAC de base de l'isoflurane fut déterminée préalablement. Une troisième détermination de la MAC a débuté 30 min après l'arrêt de la CRI. Le groupe 2 (détermination lors de jours distincts) a eu l'effet atténuant de la kétamine déterminé sans détermination préalable de MAC de base de l'isoflurane. Une deuxième détermination de la MAC fut débutée 30 min après l'arrêt de la CRI. Dans le groupe 1, la MAC d'isoflurane (2,15 ± 0,09 %) était significativement réduite par la kétamine (1,63 ± 0,07 %). Après l'arrêt de la CRI, la MAC était significativement moindre (2,04 ± 0,11 %) que la valeur de MAC de base d'isoflurane et significativement plus élevée que la MAC durant la CRI. Dans le groupe 2, la kétamine diminua la MAC d'isoflurane (1,53 ± 0,22 %) et la MAC augmenta de manière significative (1,94 ± 0,25 %) après l'arrêt de la CRI. Les valeurs de MAC n'ont pas différé significativement entre les groupes durant soit l'administration de kétamine ou après l'arrêt de kétamine. Dans les présentes conditions expérimentales, la détermination préalable de la MAC de base d'isoflurane n'a pas altéré l'effet de la kétamine sur la MAC. Les deux méthodes pour déterminer la MAC ont semblé être valides pour des besoins de recherche.(Traduit par Docteur Serge Messier).

The use of vascular access ports for blood collection in feline blood donors.

We investigated vascular access ports for feline blood donation. Eight cats were anesthetized for conventional blood collection by jugular venipuncture at the beginning and end of the study. In-between conventional collections, vascular access ports were used for collection with or without sedation every 6 to 8 wk for 6 mo. Ports remained functional except for one catheter breakage, but intermittent occlusions occurred. Systolic blood pressure was lower during conventional collection. Behavioral abnormalities occurred during 3 port collections. Packed red cells prepared from collected blood were stored at 4°C for 25 d and assessed for quality pre- and post-storage. With both collection methods, pH and glucose level declined, and potassium level, lactate dehydrogenase activity and osmotic fragility increased. There were no differences between methods in pre-storage albumin and HCO(3)(-) levels, and pre and post-storage hematocrit, lactate dehydrogenase activity, and glucose and potassium levels. Pre-storage pH and pCO(2) were higher with conventional collection, and pre- and post-storage osmotic fragility were greater with port collection. One port became infected, but all cultures of packed red cells were negative. Tissue inflammation was evident at port removal. In a second study of conventional collection in 6 cats, use of acepromazine in premedication did not exacerbate hypotension. The use of vascular access ports for feline blood donation is feasible, is associated with less hypotension, and may simplify donation, but red cell quality may decrease, and effects on donors must be considered.

Use of ephedrine and dopamine in dogs for the management of hypotension in routine clinical cases under isoflurane anesthesia.

OBJECTIVE: To determine the cardiovascular responses of ephedrine and dopamine for the management of presurgical hypotension in anesthetized dogs. STUDY DESIGN: Prospective, randomized, clinical trial. ANIMALS: Twelve healthy client-owned dogs admitted for orthopedic surgery; six per group METHODS: Prior to surgery, 58 anesthetized dogs were monitored for hypotension [mean arterial pressure (MAP) <60 mmHg] that was not associated with bradycardia or excessive anesthetic depth. Ephedrine (0.2 mg kg(-1), IV) or dopamine (5 microg kg(-1) minute(-1), IV) was randomly assigned for treatment in 12 hypotensive dogs. Ten minutes after the first treatment (Tx(1)-10), ephedrine was repeated or the dopamine infusion rate was doubled. Cardiovascular assessments taken at baseline, Tx(1)-10, and 10 minutes following treatment adjustment (Tx(2)-10) were compared for differences within and between treatments (p < 0.05). RESULTS: Ephedrine increased cardiac index (CI), stroke volume index (SVI), oxygen delivery index (DO(2)I), and decreased total peripheral resistance (TPR) by Tx(1)-10, while MAP increased transiently (<5 minutes). The second ephedrine bolus produced no further improvement. Dopamine failed to produce significant changes at 5 microg kg(-1) minute(-1), while 10 microg kg(-1) minute(-1) increased MAP, CI, SVI significantly from baseline, and DO(2)I compared with Tx(1)-10. The improvement in CI, SVI, and DO(2)I was not significantly different between treatments at Tx(2)-10. CONCLUSIONS AND CLINICAL RELEVANCE: In anesthetized hypotensive dogs, ephedrine and dopamine improved cardiac output and oxygen delivery. However, the pressure-elevating effect of ephedrine is transient, while an infusion of dopamine at 10 microg kg(-1) minute(-1) improved MAP significantly by additionally maintaining TPR.