Cardiovascular effects of desflurane in mechanically ventilated calves

OBJECTIVE: To determine cardiovascular effects of desflurane in mechanically ventilated calves. ANIMALS: 8 healthy male calves. PROCEDURE: Calves were anesthetized by face mask administration of desflurane to permit instrumentation. Administration of desflurane was temporarily discontinued until mean arterial blood pressure increased to >or= 100 mm Hg, at which time baseline cardiovascular values, pulmonary arterial temperature, end-tidal CO(2) tension, and end-tidal desflurane concentration were recorded. Cardiac index and systemic and pulmonary vascular resistances were calculated. Arterial blood gas variables were measured and calculated. Mean end-tidal concentration of desflurane at this time was 3.4%. After collection of baseline values, administration of 10% end-tidal concentration of desflurane was resumed and calves were connected to a mechanical ventilator. Cardiovascular data were collected at 5, 10, 15, 30, and 45 minutes, whereas arterial blood gas data were collected at 15 and 45 minutes after collection of baseline data. RESULTS: Mean +/- SD duration from beginning desflurane administration to intubation of the trachea was 151 +/- 32.8 seconds. Relative to baseline, desflurane anesthesia was associated with a maximal decrease in arterial blood pressure of 35% and a decrease in systemic vascular resistance of 34%. Pulmonary arterial blood temperature was decreased from 15 through 45 minutes, compared with baseline values. There were no significant changes in other measured variables. All calves recovered from anesthesia without complications. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of desflurane for induction and maintenance of general anesthesia in calves was smooth, safe, and effective. Cardiopulmonary variables remained in reference ranges throughout the study period.     

Comparative cardiovascular, analgesic, and sedative effects of medetomidine, medetomidine–hydromorphone, and medetomidine–butorphanol in dogs

The purpose of this study was to determine the cardiovascular, analgesic, and sedative effects of IV medetomidine (M, 20 µg kg^?1), medetomidine–hydromorphone (MH, 20 µg kg^?1 ? 0.1 mg kg^?1), and medetomidine–butorphanol (MB, 20 µg kg^?1 ? 0.2 mg kg^?1) in dogs. Using a randomized cross‐over design and allowing 1 week between treatments, six healthy, mixed‐breed dogs (five males and one female) weighing 20 ± 3 kg, were induced to anesthesia by face‐mask administration of 2.9% ET sevoflurane to facilitate instrumentation prior to administration of the treatment combinations. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (PAP), pulmonary arterial occlusion pressure (PAOP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output via thermodilution using 5 mL of 5% dextrose, and recording the average of the three replicate measurements. Cardiac index (CI) and systemic (SVR) and pulmonary vascular resistances were calculated. After instrumentation was completed, administration of sevoflurane was discontinued, and the dogs were allowed to recover for 30 minutes prior to administration of the treatment drugs. After collection of the baseline samples for blood gas analysis and recording the baseline cardiovascular variables, the test agents were administered IV over 10 seconds and the CV variables recorded at 5, 10, 15, 30, 45, and 60 minutes post‐injection. In addition, arterial blood was sampled for blood gas analysis at 15 and 45 minutes following injection. Intensity and duration of analgesia (assessed by toe‐pinch response using a hemostat) and level of sedation were evaluated at the above time points and at 75 and 90 minutes post‐injection. Data were analyzed using anova for repeated measures with posthoc differences between means identified using Bonferroni's method (p < 0.05). Administration of M, MH, or MB was associated with increases in SAP, MAP, DAP, PAP, PAOP, CVP, SVR, and TEMP and with decreases in HR and CI. No differences in CV variables between treatment groups were identified at any time. PaO₂ increased over time in all groups and was significantly higher when MH was compared with M. At 45 minutes, PaO₂ tended to decrease over time and was significantly lower when MH and MB were compared with M at 15 minutes. Analgesia scores for MH and MB were significantly higher compared with M through 45 minutes, while analgesia scores for MH were significantly higher compared with M through 90 minutes. Sedation scores were higher for MH and MB compared with M throughout 90 minutes. Durations of lateral recumbency were 108 ± 10.8, 172 ± 15.5, and 145 ± 9.9 minutes for M, MH, and MB, respectively. We conclude that MH and MB are associated with improved analgesia and sedation and have similar CV effects when compared with M.     

Hemodynamic Effects of Epidural Ketamine in Isoflurane-Anesthetized Dogs

Objective —The purpose of this study was to determine the hemodynamic effects of epidural ketamine administered during isoflurane anesthesia in dogs. Study Design —Prospective, single-dose trial. Animals —Six healthy dogs (five males, one female) weighing 25.3 ± 3.88 kg. Methods —Once anesthesia was induced, dogs were maintained at 1.5 times the predetermined, individual minimum alveolar concentration (MAC) of isoflurane. Dogs were instrumented and allowed to stabilize for 30 minutes before baseline measurements were recorded. Injection of 2 mg/kg of ketamine in 1 mL saline/4.5 kg body weight was then performed at the lumbosacral epidural space. Hemodynamic data were recorded at 5, 10, 15, 20, 30, 45, 60, and 75 minutes after epidural ketamine injection. Statistical analysis included an analysis of variance (ANOVA) for repeated measures over time. All data were compared with baseline values. A P < .05 was considered significant. Results —Baseline values ±standard error of the mean (X ± SEM) for heart rate, mean arterial pressure, mean pulmonary artery pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, stroke index, systemic vascular resistance, pulmonary vascular resistance, and rate-pressure product were 108 ± 6 beats/min, 85 ± 10 mm Hg, 10 ± 2 mm Hg, 3 ± 1 mm Hg, 5 ± 2 mm Hg, 2.3 ± 0.3 L/min/m², 21.4 ± 1.9 mL/beat/m², 3386 ± 350 dynes/sec/cm⁵, 240 ± 37 dynes/sec/cm⁵, and 12376 ± 1988 beats/min±mm Hg. No significant differences were detected from baseline values at any time after ketamine injection. Conclusions —The epidural injection of 2 mg/kg of ketamine is associated with minimal hemodynamic effects during isoflurane anesthesia. Clinical Relevance —These results suggest that if epidural ketamine is used for analgesia in dogs, it will induce minimal changes in cardiovascular function.     

Hemodynamic effects of sevoflurane in spontaneously breathing cats

Sevoflurane has recently been introduced in feline anesthesia. However, its cardiovascular effects have not, to our knowledge, been reported in this species. Six healthy cats, aged 1.81 ± 0.31 years (mean ± SEM) and weighing 3.47 ± 0.11 kg, were studied. Anesthesia was induced and maintained with sevoflurane in oxygen. Body temperature was maintained between 38.5 and 39.55 °C. After instrumentation, end‐tidal sevoflurane concentration was randomly set at 1.25, 1.5, and 1.75 times the individual minimum alveolar concentration (MAC), determined in a previous study, according to a Latin Square Design. Thirty minutes of stabilization was allowed after each change of concentration. ECG and heart rate, systemic and pulmonary arterial pressures, central venous pressure (CVP), and core body temperature were continuously monitored and recorded. Inspired and end‐tidal oxygen, carbon dioxide, and sevoflurane concentrations were measured using a Raman spectrometer, calibrated every 80 minutes with three calibration gases of known sevoflurane concentration (1, 2, and 5%). Moreover, at selected times, pulmonary artery occlusion pressure and cardiac output (thermodilution) were measured, and arterial and mixed venous blood samples were collected for pH and blood gas analysis, hemoglobin concentration, hemoglobin oxygen saturation, packed cell volume (PCV) and total protein determination, and lactate concentration measurement. Cardiac index (CI), stroke index (SI), systemic and pulmonary vascular resistance indices, rate‐pressure product, left and right ventricular stroke work indices (LVSWI and RVSWI, respectively), arterial and mixed venous oxygen contents, oxygen delivery, oxygen consumption, and oxygen utilization ratio were calculated. Data were analyzed by a Repeated Measure Latin Square Design followed by a Tukey's test for 2 × 2 comparisons. Arterial pH significantly decreased from 7.40 ± 0.05 to 7.29 ± 0.07 with the administration of increasing concentrations of sevoflurane. Similarly, LVSWI decreased from 3.72 ± 0.60 to 2.60 ± 0.46 g m^?2. Mean arterial pressure, PaO₂, mixed venous pH, CI, SI, and oxygen delivery tended to decrease dose‐dependently, whereas CVP, PaCO₂, Pv CO₂, PCV, and arterial and mixed venous hemoglobin concentrations tended to increase dose‐dependently with the administration of sevoflurane. However, these trends did not reach statistical significance, possibly because of the limited number of animals studied. Sevoflurane seemed to induce dose‐dependent cardiovascular depression in cats.     

The Cardiovascular Response of Sheep to Tiletamine–Zolazepam and Butorphanol Tartrate Anesthesia

Butorphanol tartrate (0.5 mg/kg intravenously [IV]) was administered to six ewes (group 1), 10 minutes before administration of tiletamine-zolazepam (12 mg/kg IV). In six ewes (group 2), butorphanol tartrate and tiletamine-zolazepam were administered simultaneously. Time of administration of butorphanol did not alter hemodynamics or duration of anesthesia significantly. Anesthesia was adequate for 25 to 45 minutes (mean, 31 min) in group 1. The sheep in group 2 were anesthetized effectively for 25 to 50 minutes (mean, 39 min). Neither dosing regimen caused significant changes in right atrial pressure, heart rate, pulmonary vascular resistance, or pulmonary capillary wedge pressure. Mean arterial blood pressure (MABP) decreased an average of 18% from baseline values of 113 mm Hg to a minimum of 84 mm Hg at minute 60 in group 1, and from 111 mm Hg to 92 mm Hg at minute 75 in group 2. The decrease was significant only for group 1. Cardiac output (CO) was significantly decreased 24% from 6.6 L/min at minute 45 in group 1, and 32% from 6.3 L/min at minute 15 in group 2. Systemic vascular resistance (SVR) was increased significantly at minute 15, 11% in group 1 and 37% in group 2. Mild respiratory acidosis was measured by significant decreases in arterial pO2 and pH and a significant increase in pCO2 without significant changes in HCO3-. Results of this study show that (1) tiletamine-zolazepam and butorphanol tartrate produce adequate anesthesia for 25 to 50 minutes; (2) the cardiovascular and anesthetic effects of the dosing schedules were similar; and (3) tiletamine-zolazepam and butorphanol result in decreased CO and MABP with a concomitant increase in SVR, and mild respiratory acidosis.     

Cardiopulmonary effects associated with head-down position in halothane-anesthetized ponies with or without capnoperitoneum

Objective To compare the cardiopulmonary effects of the head‐down position, with or without capnoperitoneum, in halothane‐anesthetized horses. Study design Prospective randomized study. Animals Five ponies (four mares, one stallion; bodyweight 302 ± 38.4 kg [mean ± SD]) were used. Methods The ponies were anesthetized with xylazine, guiafenesin, ketamine, and maintained with halothane/oxygen and lungs were ventilated to 40 ± 2 mm Hg (5.3 ± 0.3 kPa) end‐tidal CO₂ tension. After baseline cardiopulmonary measurements, ponies were kept in horizontal position for 30 minutes, then tilted head‐down 30° to the horizontal position for 60 minutes, and then returned to a horizontal position for final measurements. Capnoperitoneum (intra‐abdominal pressure: 12 mm Hg [1.6 kPa]) was introduced after baseline cardiopulmonary measurements, until 5 minutes before the final measurements (treatment INS). Ponies in the control treatment (CON) did not receive capnoperitoneum. Cardiopulmonary data were collected every 10 minutes following the baseline measurements until recovery. Results In the head‐down position, in both treatments, significant decreases were observed in PaO₂, and significant increases were observed in PaCO₂, right atrial blood pressure, arterial to end‐tidal CO₂ gradient, calculated V_d/V_t and ratios. During the head‐down position, in CON there was decreased cardiac index, and in INS, there were decreases in arterial plasma pH and increases in mean systemic arterial and airway pressures. Treatment INS developed ventilation–perfusion mismatch earlier in the study, and had longer recovery times compared to CON. Conclusion Cardiac index and systemic blood pressure appeared to be preserved in INS during the head‐down position, but ventilation–perfusion mismatch appeared earlier with head‐down position and capnoperitoneum. Clinical relevance Healthy ponies tolerate capnoperitoneum at 12 mm Hg (1.6 kPa) intra‐abdominal pressure when tilted head down 30° to the horizontal position.     

Evaluation of an indirect oscillometric blood pressure monitor in normotensive and hypotensive anesthetized dogs

Objective – To determine the accuracy and precision of an oscillometric noninvasive blood pressure device as a predictor of invasive direct blood pressure in healthy anesthetized hypotensive and normotensive dogs. Design – Prospective observational study. Setting – University teaching hospital. Animals – Eight crossbred adult dogs. Interventions – Anesthesia was induced with propofol and maintained with isoflurane. A catheter was placed in the dorsal pedal artery to record systolic, mean, and diastolic arterial blood pressures (aSAP, aMAP, and aDAP, respectively). The noninvasive blood pressure device cuff was placed around the contralateral front limb to record noninvasive systolic, mean, and diastolic blood pressure (nSAP, nMAP, and nDAP). Two states of blood pressure (BP) were studied: baseline state was established by keeping end‐tidal isoflurane concentration at 1.2±0.1%. The hypotensive state was achieved by maintaining the same isoflurane concentration while withdrawing approximately 40% of the animal's blood volume until aMAP was stable at approximately 40 mm Hg. At the end of the study, blood was returned to the animal and it was allowed to recover from anesthesia. Measurements and Main Results – Agreement between the direct and indirect BP measurements was determined by the Bland‐Altman method. The SAP and MAP but not DAP bias varied significantly between each BP state. Normotensive absolute biases (mean [SD]) for SAP, MAP, and DAP were ?14.7 mm Hg (15.5 mm Hg), ?16.4 mm Hg (12.1 mm Hg), and ?14.1 mm Hg (15.8 mm Hg), respectively. Absolute biases during the hypotensive state for SAP, MAP, and DAP were ?32 mm Hg (22.6 mm Hg), ?24.2 mm Hg (19.5 mm Hg), and ?16.8 mm Hg (17.2 mm Hg), respectively. Conclusion – The oscillometric device was not reliably predictive of intra‐arterial BP during hypotension associated with acute hemorrhage.     

Circulatory, respiratory and behavioral responses in isoflurane anesthetized llamas

Objectives To evaluate the circulatory, respiratory and behavioral effects of isoflurane (ISO) anesthesia in llamas during mechanical ventilation and spontaneous breathing. Design Prospective randomised study. Animals Six adult, neutered male llamas (10 ± 1 years [mean ± SD], 179 ± 32 kg). Materials and methods Animals in which the minimum alveolar concentration (MAC) had been previously determined were anesthetized with ISO in oxygen. Inspired and end‐tidal (ET) ISO were sampled continuously. Arterial blood pH, respiratory and circulatory variables, and clinical signs of anesthesia were recorded at three doses (1.0, 1.5 and 2.0 times the individual animal's MAC; mean MAC value 1.13%) of ISO during spontaneous and controlled ventilation. A series of Latin squares was used to determine order of dose. Controlled ventilation (CV) (target PaCO₂ 38 ± 5 mm Hg [5.0 ± 0.6 kPa]) preceded spontaneous ventilation (SV) at each dose. Animals breathed spontaneously for approximately 10 minutes prior to data collection. Body temperature was maintained at 37 ± 0.6 °C. Circulatory and respiratory data were analysed with a mixed model, least squares analysis of variance, for repeated measures taken at equally spaced intervals. p < 0.05. Results Dose and mode of ventilation had significant influences on measured variables. For example, heart rate increased as dose increased; 67 ± 14 beats minute^?1 at 1.0 MAC‐CV versus 77 ± 6 beats minute^?1 at 2 MAC‐CV. Conversely, mean arterial pressure decreased with increasing dose; 82 ± 13 mm Hg at MAC‐CV versus 52 ± 15 mm Hg at 2 MAC‐CV. Arterial CO₂ increased with increasing dose during SV; 45 ± 5 mm Hg [6 ± 0.6 kPa] at MAC versus 53 ± 4 mmHg [7 ± 0.5 kPa] at 2 MAC. Reflex activity (e.g. palpebral reflex) and muscle tone (e.g. jaw tone) decreased while eyelid aperture increased with increasing anesthetic dose. Conclusions and Clinical Relevance The influence of ISO dose and mode of ventilation on circulatory and respiratory variables in llamas is qualitatively similar to that reported in other species. Changes in reflex activity and muscle tone may be used to guide appropriate anesthetic delivery in ISO‐induced llamas.     

The Cardiopulmonary Effects of Oxymorphone in Hypovolemic Dogs

Blood was withdrawn from 15 dogs over the course of about 1 hour until the mean arterial blood pressure was reduced to 60 mm Hg. Small aliquots of additional blood were withdrawn in order to maintain the mean arterial blood pressure near 60 mm Hg for an additional hour. Oxymorphone (0.4 mg/kg) was then administered intravenously to ten dogs, and all measurements were repeated in 5, 15, 30, and 60 minutes. Five dogs served as controls.
Heart rate, tidal volume, arterial oxygen, oxygen extraction, and pH significantly decreased after oxymorphone administration, while systemic and pulmonary arterial blood pressures, systemic vascular resistance (transiently), breathing rate, minute ventilation, physiologic dead space, venous admixture, venous oxygen, arterial and venous carbon dioxide, and bicarbonate concentration increased significantly. Cardiac output was also increased, but the change was not statistically significant. Oxymorphone was associated with significantly lower heart rate, tidal volume, arterial oxygen, and pH, and higher systemic and pulmonary arterial pressure, cardiac output, venous oxygen, and arterial and venous carbon dioxide, compared to the control group, which did not receive oxymorphone.
Oxymorphone significantly improved cardiovascular performance and tissue perfusion in these hypovolemic dogs. Oxymorphone did cause a significant increase in arterial carbon dioxide and a decrease in arterial oxygenation. Oxymorphone is an opioid agonist that may represent a reasonable alternative for the induction of anesthesia in patients who are candidates for induction hypotension.     

The Hemodynamic Response of Calves to Tiletamine-Zolazepam Anesthesia

Six isoflurane-anesthetized calves were instrumented for hemodynamic studies and allowed to recover from anesthesia. When the mean arterial blood pressure rose to 100 mmHg or when vigorous movement occurred, a 1:1 tiletamine-zolazepam mixture (4 mg/kg) was administered intravenously (IV). Values for cardiac output, cardiac index, stroke index, central venous pressure, and right ventricular stroke work index did not change significantly. Systolic, mean, and diastolic arterial blood pressures and systemic vascular resistance were significantly decreased below baseline at 5 minutes; they were significantly increased above baseline at 20 minutes and remained so throughout the 60 minute study. Changes in left ventricular stroke work index and rate pressure product were similar to those of arterial blood pressure and systemic vascular resistance, although they were not significant. Heart rate and pulmonary capillary wedge pressure decreased significantly but gradually returned to baseline at 40 minutes and then increased significantly above baseline by the end of the study. Minor venous-arterial shunting or perhaps mismatching of ventilation and perfusion appeared to have developed in the later stages of the study. This was reflected in a minor increase in the arterial partial pressure of carbon dioxide (PaCO2) and a decrease in the arterial partial pressure of oxygen (PaO2) and arterial pH. At the dose administered, the hemodynamic changes induced by tiletamine-zolazepam were minimal and were compatible with safe anesthesia in calves.     

EFFECT OF SEVOFLURANE ANESTHESIA AND BLOOD DONATION ON THE SONOGRAPHIC APPEARANCE OF THE SPLEEN IN 60 HEALTHY CATS

The aims of this prospective study were to describe the normal sonographic size and appearance of the feline spleen, and to test effects of sevoflurane anesthesia and blood collection on sonographic characteristics. Sonographic evaluations were performed in 60 healthy blood donor cats prior to anesthesia and blood collection (baseline), after anesthesia induction, after completion of blood collection while under anesthesia, and 7–10 days after blood collection. Transverse sonographic images of the splenic mid‐body were made. Splenic height, width, cross‐sectional area, echogenicity relative to the left renal cortex, and echotexture were recorded. Height, width, and cross‐sectional area were compared across time periods using linear‐mixed effects models. Holm's method was applied to adjust for multiplicity and control the overall Type 1 error rate at α = 0.05. Normal transverse sonographic splenic measurements (mean ± standard deviation) at baseline were: height 8.2 ± 1.4 mm; width 26.7 ± 4.4 mm; and CSA 1.6 ± 0.5 cm². While there were statistically significant differences in splenic height, width, and cross‐sectional area after sevoflurane anesthesia and/or blood collection, differences were of low magnitude. The spleen was diffusely homogenous and subjectively isoechoic or mildly hyperechoic relative to the left renal cortex. In 77% of castrated male cats, the spleen was isoechoic to the left renal cortex. We conclude that sevoflurane anesthesia and blood donation do not subjectively alter splenic dimensions, echogenicity and echotexture in normal cats.     

Aerosolized salbutamol (albuterol) improves PaO2 in hypoxaemic anaesthetized horses – a prospective clinical trial in 81 horses

Objective To compare the arterial pH and blood gas values, heart rate and mean arterial blood pressure, in hypoxaemic anaesthetized horses, before and after treatment, with a salbutamol (albuterol) aerosol. Animal population Eighty‐one client‐owned horses weighing between 114 and 925 kg. Fifty‐seven underwent emergency abdominal surgery and 24 were anaesthetized for elective procedures. Materials and methods Pre‐anaesthetic medication included xylazine, detomidine, butorphanol and morphine, alone or in various combinations. Induction of anaesthesia was achieved with guaifenesin and ketamine, diazepam and ketamine, or guaifenesin and thiopental. The trachea of all animals was intubated and anaesthesia maintained with either halothane (33 horses) or isoflurane (48 horses) in oxygen. Heart rate and rhythm were monitored continuously. Arterial blood pressure was monitored directly, and arterial blood collected for pH and blood gas analyses. When arterial PaO₂ fell below 9.3 kPa (70 mm Hg) and failed to respond to corrective measures including positive pressure ventilation and treatment of hypotension (mean arterial blood pressures <70 mm Hg), a salbutamol aerosol (2 µg kg^?1) was delivered via the endotracheal tube. Twenty minutes later, a second arterial blood sample was analysed. Results There were no significant differences in mean arterial blood pressure, heart rate, arterial pH, base excess and bicarbonate before and after treatment. Arterial O₂ tension increased significantly from a mean ± SD of 8.3 ± 1.7 kPa (62.4 ± 13.1 mm Hg) before administration to 15.9 ± 9.8 kPa (119.4 ± 57.7 mm Hg) after treatment. There was a small but significant decrease in PaCO₂ from 7.4 ± 1.5 kPa (55.2 ± 11.2 mm Hg) to 7.0 ± 1.3 kPa (52.9 ± 9.8 mm Hg) between sample times. No changes in heart rhythm were observed. A high percentage (approximately 70%) of animals sweated following treatment. Conclusions Salbutamol administered at a dose of 2 µg kg^?1 via the endotracheal tube of anaesthetized horses with PaO₂ values less than 9.3 kPa (70 mm Hg) resulted in an almost two‐fold increase in PaO₂ values within 20 minutes of treatment. No changes in heart rate or mean arterial blood pressure were associated with the use of salbutamol in this study. The improvement in PaO₂ may be a result of bronchodilatation and improved ventilation, increased perfusion secondary to an increase in cardiac output, or a combination of these two factors. Cardiac output and ventilation–perfusion distribution were not measured in this study; therefore, the reason for the increase in PaO₂ values cannot be conclusively determined. Clinical relevance Administration of a salbutamol aerosol is a simple but effective technique that can be used to improve PaO₂ values in hypoxaemic horses during inhalant anaesthesia with no apparent detrimental side effects.     

The Komesaroff anaesthetic machine for delivering sevoflurane to dogs

Objective To quantify the vapour output of the Komesaroff machine when using sevoflurane and to determine its performance for inducing and maintaining sevoflurane anaesthesia in dogs. Study design Prospective experimental study. Animals Six clinically normal beagles, aged 3–6 years and weighing 20 ± 1.65 kg (mean ± SEM). Methods The first study was performed using five Komesaroff vaporizers to measure the sevoflurane concentration delivered at each tap setting (I to IV) at 5, 10, 15, 20, 25, 30 and 35 minutes. For this study a ventilator was connected to the Komesaroff machine and set to deliver a tidal volume of 250 mL at 10 cycles minute^?1; oxygen flow was 100 mL minute^?1. A three‐litre reservoir bag was attached to the Y‐piece connector to act as a lung model. In the second study anaesthesia was induced in dogs with sevoflurane delivered by face‐mask mask and carried in 2 L minute^?1 100% oxygen and with the vaporizer set at the fully open position. The quality and speed of induction were recorded. After orotracheal intubation, anaesthesia was maintained for 60 minutes with sevoflurane using an oxygen flow of 100 mL minute^?1. The dogs were allowed to breathe spontaneously. The respiratory rate (RR), heart rate (HR), oesophageal temperature, systolic (SAP) mean (MAP) and diastolic (DAP) arterial pressure, end‐tidal CO₂ concentration (Fe ′_CO2) end‐tidal (Fe ′_SEVO) and peak‐inspired (Fi _SEVO) percentages of sevoflurane, and vaporizer tap setting were recorded every 5 minutes during anaesthesia. Results The delivery of sevoflurane was constant for each vaporizer setting. The mean output of sevoflurane was 0.44 ± 0.01% for setting I, 2.59 ± 0.18% for setting II, 3.28 ± 0.22% for setting III and 3.1 ± 0.5% for setting IV. In the second study, the mean induction time was 7.72 ± 0.60 minutes and the quality of the induction was good in all dogs. The mean vaporizer tap setting for the maintenance of anaesthesia was 3.48 ± 0.12 and the mean values for Fe ′_SEVO and Fi _SEVO were 2.42 ± 0.04% and 2.87 ± 0.06%, respectively. The pedal withdrawal reflex persisted throughout anaesthesia. Conclusions It proved impossible to produce surgical anaesthesia with sevoflurane delivered by the Komesaroff machine despite the highest possible sevoflurane concentration being delivered. Clinical relevance Sevoflurane delivered from the Komesaroff machine cannot be relied upon to maintain surgical anaesthesia in spontaneously breathing dogs.     

Cardiorespiratory effects of a cardioselective muscarinic antagonist in anesthetized horses

Treatment of bradycardia in horses has been historically ignored because of the motility depressant effects of nonselective antimuscarinics. This study evaluated the cardiopulmonary effects of a cardioselective (M2) muscarinic antagonist, methoctramine (MET), in anesthetized horses. In a previous in vitro study, we determined that supraphysiological doses of MET were necessary to inhibit acetylcholine‐induced longitudinal jejunal smooth muscle contractions in this species. Six adult horses were allocated to two treatments in a randomized complete block design. Anesthesia was induced with xylazine/ketamine, and maintained with halothane (1% end‐tidal) and a constant infusion of xylazine (1 mg kg^?1 hour^?1) under mechanical ventilation. Invasive hemodynamic variables were monitored at baseline (approximately 45 minutes after induction) and for 120 minutes after MET or saline (control) had been injected. MET was titrated at 10‐minute intervals (10 µg kg^?1 IV) until the heart rate (HR) increased at least 30% above the baseline, or a maximum cumulative dose of 30 µg kg^?1 had been injected. A person blinded to the treatment evaluated recovery scores and monitored intestinal auscultation until 24 hours after the end of anesthesia using previously published methods. Cardiovascular parameters were analyzed by anova followed by a Dunnet's test, and nonparametrical data were analyzed by a Mann–Whitney U‐test (p < 0.05). Values were mean ± SEM unless otherwise stated. MET significantly increased HR from baseline to 120 minutes post‐injection (from 29 ± 1 to 36 ± 2 beats minute^?1 at 20 minutes). Thermodilution cardiac output (CO) and mean arterial pressure (MAP) were increased from baseline to 75 minutes post‐MET injection (from 13.9 ± 0.8 to 19.4 ± 2.0 L minute^?1 for CO at 20 minutes, and from 82 ± 3 to 103 ± 5 mm Hg for MAP at 20 minutes). Recovery characteristics and bowel auscultation scores did not differ among the groups. The return to at least 75% of the maximum auscultation score occurred at 10 (8–18) hours [median (range)] for controls and at 9 (8–12) hours for MET. It was concluded that MET increased HR and improved hemodynamic function during halothane/xylazine anesthesia with no apparent effect on return to full‐bowel motility, as assessed by auscultation. Accordingly, M2 muscarinic antagonists might be represented as a safer alternative to treat intraoperative bradycardia in horse.     

Cardiopulmonary effects of etomidate in hypovolemic dogs.

Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.     

Intravenous anaesthesia using detomidine, ketamine and guaiphenesin for laparotomy in pregnant pony mares

Objective To characterize intravenous anaesthesia with detomidine, ketamine and guaiphenesin in pregnant ponies. Animals Twelve pony mares, at 260–320 days gestation undergoing abdominal surgery to implant fetal and maternal vascular catheters. Materials and methods Pre‐anaesthetic medication with intravenous (IV) acepromazine (30 µg kg^?1), butorphanol (20 µg kg^?1) and detomidine (10 µg kg^?1) preceded induction of anaesthesia with detomidine (10 µg kg^?1) and ketamine (2 mg kg^?1) IV Maternal arterial blood pressure was measured directly throughout anaesthesia and arterial blood samples were taken at 20‐minute intervals for measurement of blood gases and plasma concentrations of cortisol, glucose and lactate. Anaesthesia was maintained with an IV infusion of detomidine (0.04 mg mL^?1), ketamine (4 mg mL^?1) and guaiphenesin (100 mg mL^?1) (DKG) for 140 minutes. Oxygen was supplied by intermittent positive pressure ventilation (IPPV) adjusted to maintain PaCO₂ between 5.0 and 6.0 kPa (38 and 45 mm Hg), while PaO₂ was kept close to 20.0 kPa (150 mm Hg) by adding nitrous oxide. Simultaneous fetal and maternal blood samples were withdrawn at 90 minutes. Recovery quality was assessed. Results DKG was infused at 0.67 ± 0.17 mL kg^?1 hour^?1 for 1 hour then reduced, reaching 0.28 ± 0.14 mL kg^?1 hour^?1 at 140 minutes. Arterial blood gas values and pH remained within intended limits. During anaesthesia there was no change in heart rate, but arterial blood pressure decreased by 10%. Plasma glucose and lactate increased (10‐fold and 2‐fold, respectively) and cortisol decreased by 50% during anaesthesia. Fetal umbilical venous pH, PO₂ and PCO₂ were 7.34 ± 0.06, 5.8 ± 0.9 kPa (44 ± 7 mm Hg) and 6.7 ± 0.8 kPa (50 ± 6 mm Hg); and fetal arterial pH, PO₂ and PCO₂ were 7.29 ± 0.06, 4.0 ± 0.7 kPa (30 ± 5 mm Hg) and 7.8 ± 1.7 kPa (59 ± 13 mm Hg), respectively. Surgical conditions were good but four ponies required a single additional dose of ketamine. Ponies took 60 ± 28 minutes to stand and recovery was good. Conclusions and clinical relevance Anaesthesia produced with DKG was smooth while cardiovascular function in mare and fetus was well preserved. This indicates that DKG infusion is suitable for maintenance of anaesthesia in pregnant equidae.     

Cardiovascular and respiratory effects of thiopental administration in hypovolemic dogs

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.     

The hemodynamic effects of intrathecal oxytocin in normal dogs

OBJECTIVE: To evaluate the hemodynamic effects produced by intrathecal administration of oxytocin in healthy isoflurane-anesthetized dogs. STUDY DESIGN: Prospective single-dose trial. ANIMAL POPULATION: Six healthy purpose-bred adult dogs weighing between 7.3 and 14.5 kg. METHODS: Dogs were anesthetized with isoflurane and instrumented. Oxytocin at a dosage of 1.6 microg/kg was administered intrathecally at the cisternal space at time 0. Hemodynamic data were recorded immediately before and at 1, 5, 15, 30, and 60 minutes after oxytocin administration. Statistical analysis included an analysis of variance (ANOVA) for repeated measures over time. A P < .05 was considered significant. RESULTS: Baseline values +/- standard error of the mean for heart rate, mean arterial pressure, central venous pressure, cardiac output, systemic vascular resistance, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, and pulmonary vascular resistance were 101 +/- 11 beats/minute, 76 +/- 7 mm Hg, 4 +/- 4 mm Hg, 1.9 +/- 0.7 L/min, 3834 +/- 2556 dynes x sec/cm5, 14 +/- 3 mm Hg, 4 +/- 2 mm Hg, and 430 +/- 201 dynes x sec/cm5, respectively. Variations from the baseline values were seen in all parameters after intrathecal oxytocin administration, but no statistically significant differences were found. CONCLUSION: The intrathecal injection of 1.6 microg/kg of oxytocin is associated with minimal hemodynamic effects during isoflurane anesthesia. CLINICAL RELEVANCE: This study revealed no clinically significant deleterious effects from the intrathecal administration of oxytocin, and investigations into its use as a perioperative analgesic are therefore warranted.     

Clinical evaluation of balanced anesthesia using infusion of midazolam–ketamine–medetomidine in combination with inhalation of sevoflurane (MKM–OS anesthesia) in horses

MKM–OS anesthesia provides general anesthesia with minimum cardiovascular depression in experimental horses. The purpose of this study was to evaluate the effect of MKM–OS anesthesia in clinical cases. Sixty‐eight horses were anesthetized with MKM–OS anesthesia for selective or emergency surgery. The horse physical status was categorized based upon the American Society of Anesthesiologists (ASA) classification scheme. Forty‐four horses were classified as ASA I or II (low‐risk; 30 soft tissue, eight ophthalmic, and six orthopedic surgeries) and 24 horses were classified as ASA III to V (high‐risk; 24 emergency colic surgeries). All horses were administered medetomidine (0.005 mg kg^–1 IV) as premedication and anesthetized with ketamine (2.5 mg kg^–1 IV) and midazolam (0.04 mg kg^–1 IV). The horses were orotracheally intubated and connected to a large animal breathing circuit that delivered oxygen‐sevoflurane and administered the midazolam (0.8 mg mL^–1)‐ketamine (40 mg mL^–1)‐medetomidine (0.05 mg mL^–1) drug combination at a rate of 0.025 mL kg^–1 hour^–1. Surgical anesthesia was maintained by controlling the dial setting of the sevoflurane vaporizer and achieved by delivering 1.6–1.8% of end‐tidal sevoflurane concentration. All horses were mechanically ventilated during anesthesia. Hypercapnia and hypoxia were not sufficiently improved in high‐risk horses (PaCO₂; low‐risk 45–53 mm Hg versus high‐risk 56–60 mm Hg, p < 0.01: PaO₂ low‐risk 248–388 mm Hg versus high‐risk 95–180 mm Hg, p < 0.01). Heart rate was significantly higher in high‐risk horses (low‐risk 37–42 bpm versus high‐risk 44–73 bpm, p < 0.01). Dobutamine infusion was required in five low‐risk (11%) and 17 high‐risk horses (68%) to maintain mean arterial blood pressure >70 mm Hg. Eleven high‐risk horses died during the perioperative period (three euthanized during surgery, two died during recovery, six died after recovery). The quality of recovery was good in low‐risk horses and good to satisfactory in high‐risk horses. MKM–OS anesthesia provided excellent surgical anesthesia with minimal to mild cardiovascular depression in low risk‐horses and mild to moderate cardiovascular depression in high risk‐horses. The possibility of preserve cardiovascular function could be the advantage of MKM–OS anesthesia in high‐risk horses.     

Cardiopulmonary Effects of Using Carbon Dioxide for Laparoscopic Surgery in Dogs

Cardiopulmonary effects of laparoscopic surgery were investigated in five crossbred dogs (21 ± 1.9 kg). Premedicated dogs were anesthetized with thiopental and maintained with halothane at 1.5 times minimum alveolar concentration in oxygen. Controlled ventilation maintained partial pressure of end-tidal co₂ at 40 ± 2 mm Hg. Vecuronium was used for skeletal muscle relaxation. After instrumentation and stabilization, baseline measurements were made of cardiac output (thermodilution technique), mean systemic, mean pulmonary arterial and pulmonary wedge pressures, heart rate, saphenous vein and central venous pressures, and minute ventilation. Baseline arterial and mixed venous blood samples were drawn for analysis of pH, Pao₂, Paco₂, Pvo₂, Pvco₂, and bicarbonate concentrations. Systemic and pulmonary vascular resistances, oxygen delivery and consumption, shunt fraction, and dead space ventilation were calculated using standard formulas. Abdominal insufflation using co₂ to a pressure of 15 mm Hg for 180 minutes resulted in significant ( P <.05) increases in heart rate (15 to 180 minutes), minute ventilation (75 to 135 minutes), and saphenous vein pressure (15 to 180 minutes), and decreases in pH (60 to 180 minutes) and Pao₂ (60 to 180 minutes). For 30 minutes after desufflation, there was a significant decrease in Pao₂, and increases in cardiac output, o₂ delivery, and heart rate, compared with baseline. There was a significant increase in shunt fraction and decrease in pH at 15 minutes after desufflation only. The changes were within physiologically acceptable limits in these healthy, ventilated dogs.