Isoflurane-anesthetized Dogs Research Articles

Electroencephalographic and Cardiovascular Assessments of Isoflurane-Anesthetized Dogs.

This study investigated the use of frontal electroencephalography (EEG) to monitor varying levels of isoflurane anesthesia in dogs. The patient state index (PSI), burst suppression ratio (SR), and waveforms, were continuously recorded while mean arterial blood pressure (MBP), heart rate, responses to electric stimuli, and subjective anesthetic "depth" were assessed every 3 min. At deep anesthesia (2.5× MAC - 3.2%), the PSI (6.5 ± 10.8) and MBP (45.6 ± 16.4 mmHg) were the lowest, and SR was the highest (78.3 ± 24.0%). At 1× MAC (1.3%), the PSI and MBP increased significantly to 47.8 ± 12.6 and 99.8 ± 13.2, respectively, and SR decreased to 0.5 ± 2.5%. The EEG was predominantly isoelectric at 2×-2.5× MAC, indicating unconsciousness and unresponsiveness. As anesthesia lightened, waveforms transitioned to flatter and faster activity patterns with a response to noxious stimuli, suggesting regained consciousness. The PSI and MBP exhibited a stronger correlation (ρ = 0.8098, p = 0.001) than the relationship of PSI with heart rate (ρ = -0.2089, p = 0.249). Five of the six dogs experienced rough recovery, possibly due to high SR and low MBP. These findings suggest that EEG monitoring in dogs can be a valuable tool for the real-time tracking of brain states and can be used to guide the management of isoflurane anesthesia.

Transpulmonary cardiac output with room temperature saline is accurate and tracks directional changes in anesthetized dogs.

To assess the performance of transpulmonary thermodilution (TPTD) using room-temperature saline (CORT) and waveform-derived continuous CO (CCO) compared with TPTD using iced saline (COICED) as the indicator for measurements of CO in isoflurane-anesthetized dogs. 8 Beagles aged 1 to 2 years (7.4 to 11.2 kg) were enrolled in this experimental study from March 21 to 31, 2023. Dogs were anesthetized with 0.01 mg/kg acepromazine, 5 to 6 mg/kg propofol, and isoflurane and were mechanically ventilated. Dogs were instrumented with a central venous catheter and a femoral arterial catheter equipped with a thermistor. The COICED, CORT, and pulse wave-derived CCO values were obtained at baseline, during infusions of phenylephrine and norepinephrine, and during blood withdrawal and replacement. Data were analyzed with a mixed effect model, Bland-Altman plots, and concordance. Percent error was calculated. P < .05 was used for significance. Data were collected from 8 dogs. Significant effects of time and the interaction of time and method were found. Bland-Altman plots showed negligible bias with limits of agreement between -0.35 and 0.25 L/min for CORT versus COICED and -1.23 and 1.15 L/min for CCO versus COICED. Percent errors were 17.7% and 66.6%, respectively. In the 4-quadrant plots, the concordance rate was 95% and 68% for measurements obtained with CORT and for CCO, respectively. Transpulmonary thermodilution using room temperature saline was accurate and able to track changes in CO. Continuous CO had a large percent error and low tracking ability. Transpulmonary thermodilution using room temperature saline is reliable for monitoring CO and obviates the need for iced preparations in clinical scenarios.

Performance of four cardiac output monitoring techniques vs. intermittent pulmonary artery thermodilution during a modified passive leg raise maneuver in isoflurane-anesthetized dogs.

This study investigated the performance among four cardiac output (CO) monitoring techniques in comparison with the reference method intermittent pulmonary artery thermodilution (iPATD) and their ability to diagnose fluid responsiveness (FR) during a modified passive leg raise (PLRM) maneuver in isoflurane-anesthetized dogs undergoing acute blood volume manipulations. The study also examined the simultaneous effect of performing the PLRM on dynamic variables such as stroke distance variation (SDV), peak velocity variation (PVV), and stroke volume variation (SVV). Prospective, nonrandomized, crossover design. Six healthy male Beagle dogs. The dogs were anesthetized with propofol and isoflurane and mechanically ventilated under neuromuscular blockade. After instrumentation, they underwent a series of sequential, nonrandomized steps: Step 1: baseline data collection; Step 2: removal of 33 mL kg-1 of circulating blood volume; Step 3: blood re-transfusion; and Step 4: infusion of 20 mL kg-1 colloid solution. Following a 10-min stabilization period after each step, CO measurements were recorded using esophageal Doppler (EDCO), transesophageal echocardiography (TEECO), arterial pressure waveform analysis (APWACO), and electrical cardiometry (ECCO). Additionally, SDV, PVV, and SVV were recorded. Intermittent pulmonary artery thermodilution (iPATDCO) measurements were also recorded before, during, and after the PLRM maneuver. A successful FR diagnosis made using a specific test indicated that CO increased by more than 15% during the PLRM maneuver. Statistical analysis was performed using one-way analysis of variance for repeated measures with post hoc Tukey test, linear regression, Lin's concordance correlation coefficient (ρc), and Bland-Altman analysis. Statistical significance was set at p < 0.05. All techniques detected a reduction in CO (p < 0.001) during hemorrhage and an increase in CO after blood re-transfusion and colloid infusion (p < 0.001) compared with baseline. During hemorrhage, CO increases with the PLRM maneuver were as follows: 33% for iPATD (p < 0.001), 19% for EC (p = 0.03), 7% for APWA (p = 0.97), 39% for TEE (p < 0.001), and 17% for ED (p = 0.02). Concurrently, decreases in SVV, SDV, and PVV values (p < 0.001) were also observed. The percentage error for TEE, ED, and EC was less than 30% but exceeded 55% for APWA. While TEECO and ECCO slightly underestimated iPATDCO values, EDCO and APWACO significantly overestimated iPATDCO values. TEE and EC exhibited good and acceptable agreement with iPATD. However, CO measurements using all four techniques and iPATD did not differ before, during, and after PLRM at baseline, blood re-transfusion, and colloid infusion. iPATD, EC, TEE, and ED effectively assessed FR in hypovolemic dogs during the PLRM maneuver, while the performance of APWA was unacceptable and not recommended. SVV, SDV, and PVV could be used to monitor CO changes during PLRM and acute blood volume manipulations, suggesting their potential clinical utility.

Phenylephrine and norepinephrine increase blood pressure through opposing physiologic mechanisms in isoflurane-anesthetized dogs receiving acepromazine.

To elucidate the cardiovascular effects of escalating doses of phenylephrine and norepinephrine in dogs receiving acepromazine and isoflurane. 8 beagles aged 1 to 2 years (7.4 to 11.2 kg). All dogs received acepromazine 0.01 mg/kg, propofol 4 to 5 mg/kg, and isoflurane and were mechanically ventilated. Mean arterial pressure (MAP) from a femoral artery catheter and continuous electrocardiogram were recorded. Cardiac output (CO) was measured with transpulmonary thermodilution. Systemic vascular resistance (SVR), global end-diastolic volume (GEDV), and global ejection fraction (GEF) were subsequently calculated. Phenylephrine and norepinephrine were infused in random order at 0.07, 0.3, 0.7, and 1.0 μg/kg/min. All variables were measured after 15 minutes of each infusion rate. The effects of dose, agent, and their interaction on the change of each variable were evaluated with mixed-effect models. A P < .05 was used for significance. Atrial premature complexes occurred in 3 dogs during norepinephrine infusion at doses of 0.3, 0.7, and 1 μg/kg/min; no dysrhythmias were seen with phenylephrine administration. MAP increased during dose escalation (P < .0001) within each agent and did not differ between agents (P = .6). The decrease in HR was greater for phenylephrine (P < .0001). Phenylephrine decreased CO and GEF and increased GEDV and SVR (all P < .03). Norepinephrine decreased the SVR and increased CO, GEDV, and GEF (all P < .03). Our results confirm that phenylephrine increases arterial pressures mainly through vasoconstriction in acepromazine-premedicated dogs while norepinephrine, historically considered a vasopressor, does so primarily through an increase in inotropism.

Characterization of electropharmacological profile of an anti-atrial fibrillatory drug vernakalant along with potential risk toward torsade de pointes: Translational studies using isoflurane-anesthetized dogs and isolated rat aortic preparations

We simultaneously assessed electropharmacological effects of anti-atrial fibrillatory drug vernakalant and its potential risk toward torsade de pointes. Vernakalant hydrochloride in doses of 0.3 and 3 mg/kg/10 min was intravenously administered to isoflurane-anesthetized beagle dogs without (n = 5) and with (n = 4) α-adrenoceptor blockade. Its vascular effect was analyzed using the rat aortae (n = 12). Vernakalant increased total peripheral vascular resistance and preload to left ventricle, leading to transient elevation of mean blood pressure indirectly via non-adrenergic pathway. Vernakalant suppressed sinus automaticity, ventricular contractility and intra-atrial/atrioventricular nodal/intraventricular conductions, and decreased cardiac output. Moreover, vernakalant prolonged atrial/ventricular effective refractory period by 53/55 ms, respectively, whereas it delayed ventricular repolarization in a reverse frequency-dependent manner. The extent of prolongation in early/late ventricular repolarization and electrically vulnerable period was 26/32 and 9 ms, respectively when QT-interval prolongation was the greatest. We compared them with those of known anti-atrial fibrillatory drugs; ranolazine, amiodarone, dronedarone, dl-sotalol and bepridil. The magnitude of vernakalant to alter those variables was the greater among those drugs except that the atrial selectivity was the lesser of those. Thus, vernakalant is expected to be efficacious against atrial fibrillation, but caution should be excised on its use for patients having labile ventricular function and repolarization.

Agreement between Electrical Cardiometry and Pulmonary Artery Thermodilution for Measuring Cardiac Output in Isoflurane-Anesthetized Dogs.

In animals, invasive pulmonary artery thermodilution (PATD) is a gold standard for cardiac output (CO) monitoring, but it is impractical in clinical settings. This study evaluates the agreement between PATD and noninvasive electrical cardiometry (EC) for measuring CO and analyzes the other EC-derived hemodynamic variables in six healthy anesthetized dogs subjected to four different hemodynamic events in a sequential order: (1) euvolemia (baseline); (2) hemorrhage (33% blood volume loss); (3) autologous blood transfusion; and (4) 20 mL/kg colloid bolus. The CO measurements obtained using PATD and EC are compared using Bland-Altman analysis, Lin's concordance correlation (LCC), and polar plot analysis. Values of p < 0.05 are considered significant. The EC measurements consistently underpredict the CO values as compared with PATD, and the LCC is 0.65. The EC's performance is better during hemorrhage, thus indicating its capability in detecting absolute hypovolemia in clinical settings. Even though the percentage error exhibited by EC is 49.4%, which is higher than the standard (<30%), EC displays a good trending ability. Additionally, the EC-derived variables display a significant correlation with the CO measured using PATD. Noninvasive EC may have a potential in monitoring trends in hemodynamics in clinical settings.

Reverse Trendelenburg position and the incidence of gastroesophageal reflux in isoflurane-anesthetized dogs

Introduction: The incidence of gastroesophageal reflux (GER) in anesthetized dogs warrants investigation into perioperative preventative strategies. This study aimed to determine if a reverse Trendelenburg position (RT) would decrease the incidence of GER compared to a horizontal position (HP) in anesthetized dogs.

Electropharmacological characterization of anti-atrial fibrillatory drug vernakalant using the isoflurane-anesthetized dogs

Electropharmacological characterization of anti-atrial fibrillatory drug vernakalant using the isoflurane-anesthetized dogs

Effect of fentanyl, with or without treatment of bradycardia, on the minimum alveolar concentration of isoflurane and cardiovascular function in dogs

ObjectiveTo determine the effect of fentanyl on the minimum alveolar concentration of isoflurane (MACISO) and cardiovascular variables in dogs, and how the treatment of bradycardia affects them. Study designProspective, randomized crossover-controlled trial. AnimalsA total of six male Beagle dogs weighing 9.9 ± 0.7 kg (mean ± standard deviation) and aged 13 months. MethodsTo each dog, two treatments were assigned on different days: fentanyl (FENTA) or fentanyl plus glycopyrrolate (FENTAglyco) to maintain heart rate (HR) between 100 and 132 beats minute−1. Determinations of MACISO were performed with 10 plasma fentanyl target concentrations ([Fenta]Target (0, 0.16, 0.32, 0.64, 1.25, 2.5, 5.0, 10.0, 20.0 and 40.0 ng mL−1) for FENTA and 5 [Fenta]Target (0, 1.25, 2.5, 5.0, 10.0 ng mL−1)) for FENTAglyco. During each MACISO determination, cardiovascular variables [mean arterial pressure (MAP), HR and cardiac index (CI)] were measured, and systemic vascular resistance index (SVRI) calculated. Pharmacodynamic models were used to describe the plasma fentanyl concentration [Fenta]–response relationship for the effect on MACISO and cardiovascular variables. A mixed-model analysis of variance followed by Dunnett’s or Tukey’s test, and the Bonferroni adjustment were used for comparisons within and between each treatment, respectively. Significance was set as p < 0.05. ResultsFentanyl decreased MACISO by a maximum of 84%. The [Fenta] producing 50% decrease in MAC, HR and CI were 2.64, 3.65 and 4.30 ng mL−1 (typical values of population model), respectively. The prevention of fentanyl-mediated bradycardia caused no significant effect on MACISO, but increased HR, MAP and CI, and decreased SVRI when compared with isoflurane alone. Conclusions and clinical relevanceFentanyl caused a plasma concentration-dependent decrease in MACISO, HR and CI and an increase in SVRI. Cardiovascular improvements associated with fentanyl in isoflurane-anesthetized dogs only occurred when the fentanyl-mediated bradycardia was prevented.

Cardiovascular function, pulmonary gas exchange and tissue oxygenation in isoflurane-anesthetized, mechanically ventilated Beagle dogs with four levels of positive end-expiratory pressure

ObjectivesTo compare pulmonary gas exchange, tissue oxygenation and cardiovascular effects of four levels of end-expiratory pressure: no positive end-expiratory pressure (ZEEP), positive end-expiratory pressure (PEEP) of maximal respiratory system compliance (PEEPmaxCrs), PEEPmaxCrs + 2 cmH2O (PEEPmaxCrs+2), PEEPmaxCrs + 4 cmH2O (PEEPmaxCrs+4), in isoflurane-anesthetized dogs. Study designProspective randomized crossover study. AnimalsA total of seven healthy male Beagle dogs, aged 1 year and weighing 10.2 ± 0.7 kg (mean ± standard deviation). MethodsThe dogs were administered acepromazine and anesthesia was induced with propofol and maintained with isoflurane. Ventilation was controlled for 4 hours with ZEEP, PEEPmaxCrs, PEEPmaxCrs+2 or PEEPmaxCrs+4. Cardiovascular, pulmonary gas exchange and tissue oxygenation data were evaluated at 5, 60, 120, 180 and 240 minutes of ventilation and compared using a mixed-model anova followed by Bonferroni test. p < 0.05 was considered significant. ResultsCardiac index (CI) and mean arterial pressure (MAP) were lower in all PEEP treatments at 5 minutes when compared with ZEEP. CI persisted lower throughout the 4 hours only in PEEPmaxCrs+4 with the lowest CI at 5 minutes (2.15 ± 0.70 versus 3.45 ± 0.94 L minute–1 m–2). At 180 and 240 minutes, MAP was lower in PEEPmaxCrs+4 than in PEEPmaxCrs, with the lowest value at 180 minutes (58 ± 7 versus 67 ± 7 mmHg). Oxygen delivery index (DO2I) was lower in PEEPmaxCrs+4 than in ZEEP at 5, 60, 120 and 180 minutes. Venous admixture was not different among treatments. Conclusion and clinical relevanceThe use of PEEP caused a transient decrease in MAP and CI in lung-healthy dogs anesthetized with isoflurane, which improved after 60 minutes of ventilation in all levels of PEEP except PEEPmaxCrs+4. A clinically significant improvement in arterial oxygenation and DO2I was not observed with PEEPmaxCrs and PEEPmaxCrs+2 in comparison with ZEEP, whereas PEEPmaxCrs+4 decreased DO2I.

Evaluation of the analgesic effect of fentanyl–ketamine and fentanyl–lidocaine constant rate infusions in isoflurane-anesthetized dogs undergoing thoracolumbar hemilaminectomy

ObjectiveTo evaluate anesthetic conditions and postoperative analgesia with the use of intraoperative constant rate infusions (CRIs) of fentanyl–lidocaine or fentanyl–ketamine in dogs undergoing thoracolumbar hemilaminectomy. Study designProspective, randomized, blinded, clinical study. AnimalsA total of 32 client-owned dogs. MethodsDogs were premedicated with fentanyl (5 μg kg–1) administered intravenously (IV), anesthesia was induced with IV alfaxalone and maintained with isoflurane. Fentanyl (0.083 μg kg–1 minute–1) was infused IV with either ketamine (0.5 mg kg–1; then 40 μg kg–1 minute–1; group KF) or lidocaine (2 mg kg–1; then 200 μg kg–1 minute–1; group LF) assigned randomly. Heart rate, noninvasive arterial pressures, respiratory rate, esophageal temperature, end-tidal partial pressure of carbon dioxide and isoflurane concentration were recorded throughout anesthesia. Maintenance of anesthesia, recovery and postoperative pain (Glasgow Composite Pain Scale) were scored. Cardiopulmonary data were analyzed using a two-way anova with repeated measures, demographics of the two groups with a t test, and scores with Mann–Whitney U test, with p < 0.05. ResultsAll dogs recovered from anesthesia without complications. No significant difference was found between groups for cardiopulmonary variables, total anesthesia time, sedation score and requirement for postoperative sedation or for rescue analgesia. Anesthetic maintenance score was of lower quality in KF than in LF [median (interquartile range): 0 (0–0.5) versus 0 (0–0); p = 0.032)], but still considered ideal. Recovery score was higher and indicative of less sedation in LF than in KF [1 (1–1.5) versus 0.5 (0–1); p < 0.0001]. Pain score was higher in KF than in LF [2 (1–3) versus 1 (1–2); p = 0.0009]. Conclusions and clinical relevanceBoth CRIs of KF and LF provided adequate anesthetic conditions in dogs undergoing thoracolumbar hemilaminectomy. Based on requirement for rescue analgesia, postoperative analgesia was adequate in both groups.

Use of aortic flow indexes derived from transthoracic echocardiography to evaluate response to a fluid challenge in anesthetized dogs

ObjectiveTo evaluate the ability of transthoracic echocardiographic aortic flow measurements to discriminate response to a fluid challenge (FC) in healthy anesthetized dogs. Study designProspective experimental study. AnimalsA total of 48 isoflurane-anesthetized dogs (14.2–35.0 kg) undergoing elective surgery. MethodsFluid responsiveness was evaluated before surgery by FC (lactated Ringer’s 10 mL kg–1 intravenously over 5 minutes). Percentage increases in transpulmonary thermodilution stroke volume (ΔSVTPTD) >15% from values recorded before FC defined responders to volume expansion. A group of 24 animals were assigned as nonresponders (ΔSVTPTD ≤15%). When ΔSVTPTD was >15% after the first FC, additional FC were administered until ΔSVTPTD was ≤15%. Final fluid responsiveness status was based on the response to the last FC. Percentage increases after FC in aortic flow indexes [velocity time integral (ΔVTIFC) and maximum acceleration (ΔVmaxFC)] and in mean arterial pressure (ΔMAPFC) were compared with ΔSVTPTD. ResultsAfter one FC, 24 animals were responders. For nonresponders, ΔSVTPTD was ≤15% after one, two and three FCs in eight/24, 15/24 and one/24 animals, respectively. The FC that defined responsiveness increased ΔSVTPTD by 29 (18–53)% in responders and by 8 (–3 to 15)% in nonresponders [mean (range)]. The area under the receiver operating characteristics curve (AUROC) of ΔVTIFC (0.901) was larger than the AUROCs of ΔVmaxFC (0.774, p = 0.041) and ΔMAPFC (0.519, p < 0.0001). ΔMAPFC did not predict responsiveness (p = 0.826). Best cut-off thresholds for discriminating responders, with respective zones of diagnostic uncertainty (gray zones) were >14.7 (10.8–17.6)% for ΔVTIFC and >8.6 (–0.3 to 14.7)% for ΔVmaxFC. Animals within the gray zone were 17% (ΔVTIFC) and 50% (ΔVmaxFC). Conclusions and clinical relevanceChanges in VTI induced by FC can determine responsiveness with reasonable accuracy in dogs and could play an important role in goal-directed fluid therapy.

Effect of administering dexmedetomidine with or without atropine on cardiac troponin I level in isoflurane-anesthetized dogs

We aimed to determine whether dexmedetomidine administration with or without atropine increases cardiac troponin I (cTnI) level in healthy dogs. We hypothesized that 10 µg/kg dexmedetomidine + atropine increases the cTnI level, whereas 5 µg/kg dexmedetomidine + atropine does not. Eighteen healthy, pet dogs that underwent an orthopedic surgery or ovariohysterectomy were included in this study. The dogs were randomly assigned to atropine (0.02 mg/kg)–dexmedetomidine (10 µg/kg), saline–dexmedetomidine (10 µg/kg), and atropine (0.02 mg/kg)–dexmedetomidine (5 µg/kg) groups. Each dog was premedicated with atropine or saline intramuscularly (IM). After 10 min, they were IM injected with dexmedetomidine (10 or 5 µg/kg)–morphine (0.5 mg/kg)–midazolam (0.2 mg/kg). Following this, anesthesia was induced after 10 min with propofol and maintained with isoflurane in 100% oxygen. The median plasma cTnI level at 6, 12 and 24 hr after premedication was significantly higher than that at baseline. The cTnI level in the atropine–dexmedetomidine (10 µg/kg) group was significantly higher than that in the saline–dexmedetomidine (10 µg/kg) and atropine–dexmedetomidine (5 µg/kg) groups at 6 and 12 hr after premedication. The cTnI level returned to normal within 72 hr after premedication in all groups. The administration of atropine in combination with 10 µg/kg dexmedetomidine increased the cTnI level, indicating subclinical myocardial damage.

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs

ObjectiveTo assess cardiopulmonary function in sedated and anesthetized dogs administered intravenous (IV) dexmedetomidine and subsequently administered IV lidocaine to treat dexmedetomidine-induced bradycardia. Study designProspective, randomized, crossover experimental trial. AnimalsA total of six purpose-bred female Beagle dogs, weighing 9.1 ± 0.6 kg (mean ± standard deviation). MethodsDogs were randomly assigned to one of three treatments: dexmedetomidine (10 μg kg–1 IV) administered to conscious (treatments SED1 and SED2) or isoflurane-anesthetized dogs (end-tidal isoflurane concentration 1.19 ± 0.04%; treatment ISO). After 30 minutes, a lidocaine bolus (2 mg kg–1) IV was administered in treatments SED1 and ISO, followed 20 minutes later by a second bolus (2 mg kg–1) and a 30 minute lidocaine constant rate infusion (L-CRI) at 50 (SED1) or 100 μg kg–1 minute–1 (ISO). In SED2, lidocaine bolus and L-CRI (50 μg kg–1 minute–1) were administered 5 minutes after dexmedetomidine. Cardiopulmonary measurements were obtained after dexmedetomidine, after lidocaine bolus, during L-CRI and 30 minutes after discontinuing L-CRI. A mixed linear model was used for comparisons within treatments (p < 0.05). ResultsWhen administered after a bolus of dexmedetomidine, lidocaine bolus and L-CRI significantly increased heart rate and cardiac index, decreased mean blood pressure, systemic vascular resistance index and oxygen extraction ratio, and did not affect stroke volume index in all treatments. Conclusion and clinical relevanceLidocaine was an effective treatment for dexmedetomidine-induced bradycardia in healthy research dogs.

Hemodynamic effects of incremental doses of acepromazine in isoflurane-anesthetized dogs

ObjectiveTo evaluate the effects of incremental doses of acepromazine on hemodynamics in isoflurane-anesthetized dogs. Study designProspective, experimental study. AnimalsHealthy, adult, mixed-breed dogs (two male and four female) weighing 16.8 ± 5.1 kg (mean ± standard deviation). MethodsDogs were anesthetized with propofol (7 mg kg–1) intravenously (IV) and isoflurane. Thermodilution and arterial catheters were placed for hemodynamic monitoring and arterial blood sampling for blood gas analysis. Baseline measurements were performed with stable expired concentration of isoflurane (Fe′Iso) at 1.8%. Each dog was then administered four incremental acepromazine injections (10, 15, 25 and 50 μg kg–1) IV, and measurements were repeated 20 minutes after each acepromazine injection with Fe′Iso decreased to 1.2%. The four acepromazine injections resulted in cumulative doses of 10, 25, 50 and 100 μg kg–1 (time points ACP10, ACP25, ACP50 and ACP100, respectively). ResultsCompared with baseline, cardiac index (CI) increased significantly by 34%, whereas systemic vascular resistance index (SVRI) decreased by 25% at ACP50 and ACP100. Arterial oxygen content (CaO2) was significantly lower than baseline after all acepromazine injections (maximum decreases of 11%) and was lower at ACP50 and ACP100 than at ACP10. No significant change was found in heart rate, stroke index, oxygen delivery index and systolic, mean and diastolic blood pressures. Hypotension (mean arterial pressure < 60 mmHg) was observed in one dog at baseline, ACP10, ACP25 and ACP100, and in two dogs at ACP50. Conclusions and clinical relevanceCompared with isoflurane alone, anesthesia with acepromazine–isoflurane resulted in increased CI and decreased SVRI and CaO2 values. These effects were dose-related, being more pronounced at ACP50 and ACP100. Under the conditions of this study, acepromazine administration did not change blood pressure.

Effect of a heat and moisture exchanger on temperature and humidity of inhaled gas in isoflurane-anesthetized dogs

ObjectiveTo investigate the effects of a heat and moisture exchanger (HME) on the temperature and humidity of inhaled gas in isoflurane-anesthetized dogs. Study designProspective, interventional study. AnimalsA total of four experimental dogs and four client-owned dogs weighing 13.9 ± 7.4 kg (mean ± standard deviation). MethodsThe four experimental dogs were anesthetized on two occasions with and without an intact HME at least 1 week apart. The four client-owned dogs were anesthetized once only for a surgical procedure and assigned to the HME group or no-HME group in alternate order, resulting in six dogs for each group. All dogs were premedicated, anesthetized with propofol and intubated. The HME was connected to the endotracheal tube. Anesthesia was maintained with isoflurane. A digital thermo-hygrometer was placed between the endotracheal tube and HME. The temperature and relative humidity of the inhaled gas were measured every 5 minutes for 60 minutes and the absolute humidity was calculated at each time point. ResultsThe temperature and absolute humidity of the inhaled gas was significantly higher at 5–60 minutes after intubation in the HME group than in the no-HME group. Absolute humidity was maintained above 29 mg H2O L−1 in the HME group. No significant time-dependent effects on temperature, relative humidity or absolute humidity of the inhaled gas were observed. Conclusions and clinical relevanceThe temperature and absolute humidity of the inhaled gas were higher when an HME was used during isoflurane anesthesia in dogs. The use of an HME may reduce the risk of dehydration and dysfunction of the airway mucosal epithelium.

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and isoflurane-anesthetized dogs

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and isoflurane-anesthetized dogs

Investigation of associations between preoperative acepromazine or dexmedetomidine administration and development of arterial hypotension or bradycardia in dogs undergoing ovariohysterectomy.

OBJECTIVE To evaluate potential associations between preanesthetic administration of acepromazine or dexmedetomidine and development of arterial hypotension or bradycardia in isoflurane-anesthetized dogs undergoing ovariohysterectomy. ANIMALS 341 dogs. PROCEDURES Medical records were searched to identify dogs that underwent ovariohysterectomy between January 2009 and December 2010 and received hydromorphone with acepromazine or dexmedetomidine as preanesthetic agents. Demographic data, sedative and anesthetic drugs, duration of anesthesia, average vaporizer setting, positive pressure ventilation, occurrence of hypotension (mean arterial pressure < 60 mm Hg) or bradycardia (> 50% reduction in heart rate, compared with the preanesthetic value), time to first occurrence and duration of hypotension, and treatment with dopamine or anticholinergic agents were recorded. Data were compared between dogs that received acepromazine and dexmedetomidine. Logistic regression was used to investigate associations between the treatments of interest (and other putative risk factors) and development of hypotension or bradycardia. RESULTS For dogs that received acepromazine, the odds of developing hypotension were 2.61 times those for dogs that received dexmedetomidine. Hypotension occurred earlier and lasted longer in dogs that received acepromazine, and this group was treated with dopamine more frequently than the group that received dexmedetomidine. Lower body weight was associated with increased odds of hypotension. Odds of developing bradycardia were greater for dogs sedated with dexmedetomidine (vs acepromazine) and for dogs that underwent anesthetic induction with propofol or a ketamine-benzodiazepine combination (vs thiopental). CONCLUSIONS AND CLINICAL RELEVANCE Anesthetic complications differed between isoflurane-anesthetized dogs undergoing ovariohysterectomy after premedication with acepromazine or dexmedetomidine in this study; future prospective investigations are warranted to investigate these effects in other, less homogenous populations of dogs.

Effect of heart rate on the pharmacokinetics of fentanyl in dogs anesthetized with isoflurane and hydromorphone

ObjectiveTo compare the pharmacokinetics of fentanyl at lower (LHR) or higher heart rate (HHR) in dogs anesthetized with isoflurane. Study designProspective, randomized, crossover controlled trial. AnimalsA group of six healthy 13-month-old male Beagle dogs weighing 9.9 ± 0.7 kg (mean ± standard deviation). MethodsDogs were allocated to two treatments: LHR (HR: 45–75 beats minute−1) and HHR (HR: 100–130 beats minute−1). Anesthesia was maintained with isoflurane and hydromorphone (0.1 mg kg−1 followed by 0.02–0.10 mg kg−1 hour−1) for both treatments. Glycopyrrolate was administered in HHR to maintain HR within the desired range. Afterwards, fentanyl (20 μg kg−1) was intravenously administered over 5 minutes. Arterial blood samples were collected for plasma fentanyl concentration measurement by liquid chromatography/mass spectrometry. The pharmacokinetics of fentanyl were compared between treatments and the differences were considered significant at p < 0.05. ResultsA three-compartment model best fitted the changes in plasma fentanyl concentration. Clearance (CL; mL minute−1 kg−1) was 33.2 (24.0–48.0) and 61.3 (44.5–72.7), maximum concentration (ng mL−1) 33.6 (23.4–36.6) and 20.0 (16.7–28.0), apparent volume of the rapid peripheral compartment (mL kg−1) 436 (352–723) and 925 (499–1887), apparent volume at steady state (mL kg−1) 4064 (3453–6546) and 7195 (5077–8601), cardiac index (CI; mL minute−1 m−2) 2.83 (1.98–3.67) and 4.91 (3.22–6.09) and HR (beats minute−1) 68 (49–72) and 120 (102–129) for LHR and HHR, respectively, with significant differences between treatments. Significant correlations (0.92 and 0.90) were found between CI and CL, and between HR and CL, respectively. Conclusions and clinical relevanceThe increase in HR and the resultant improvement in cardiac output increased fentanyl CL and volume of distribution, which resulted in a decrease in plasma fentanyl concentration in isoflurane-anesthetized dogs.

Use of a novel functional bed sheet to monitor heart rate and respiratory rate of six isoflurane-anesthetized dogs

Introduction: A functional bed sheet monitor is a novel technology that was used with standard anesthetic monitoring in six dogs to assess measurement of heart rate (HR) and respiratory rate (RR). The functional bed sheet contains a sensing thread that captures information by contact, and communicates with a computer and monitor for viewing data. The functional bed sheet has potential for recording HR and RR noninvasively in anesthetized dogs. This is proof of concept for new technology.