Hemodynamic effects of carbon dioxide during intermittent positive-pressure ventilation in horses

The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2, 35 to 45 mm of Hg), moderate hypercapnia (PaCO2, 60 to 70 mm of Hg), and severe hypercapnia (PaCO2, 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P less than 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the beta-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.     

Influence of gastrointestinal tract disease on pharmacokinetics of lidocaine after intravenous infusion in anesthetized horses

OBJECTIVE: To determine the disposition of lidocaine after IV infusion in anesthetized horses undergoing exploratory laparotomy because of gastrointestinal tract disease. ANIMALS: 11 horses (mean +/- SD, 10.3 +/- 7.4 years; 526 +/- 40 kg). PROCEDURE: Lidocaine hydrochloride (loading infusion, 1.3 mg/kg during a 15-minute period [87.5 microg/kg/min]; maintenance infusion, 50 microg/kg/min for 60 to 90 minutes) was administered IV to dorsally recumbent anesthetized horses. Blood samples were collected before and at fixed time points during and after lidocaine infusion for analysis of serum drug concentrations by use of liquid chromatography-mass spectrometry. Serum lidocaine concentrations were evaluated by use of standard noncompartmental analysis. Selected cardiopulmonary variables, including heart rate (HR), mean arterial pressure (MAP), arterial pH, PaCO2, and PaO2, were recorded. Recovery quality was assessed and recorded. RESULTS: Serum lidocaine concentrations paralleled administration, increasing rapidly with the initiation of the loading infusion and decreasing rapidly following discontinuation of the maintenance infusion. Mean +/- SD volume of distribution at steady state, total body clearance, and terminal half-life were 0.70 +/- 0.39 L/kg, 25 +/- 3 mL/kg/min, and 65 +/- 33 minutes, respectively. Cardiopulmonary variables were within reference ranges for horses anesthetized with inhalation anesthetics. Mean HR ranged from 36 +/- 1 beats/min to 43 +/- 9 beats/min, and mean MAP ranged from 74 +/- 18 mm Hg to 89 +/- 10 mm Hg. Recovery quality ranged from poor to excellent. CONCLUSIONS AND CLINICAL RELEVANCE: Availability of pharmacokinetic data for horses with gastrointestinal tract disease will facilitate appropriate clinical dosing of lidocaine.     

Monitoring of the ventilatory status of anesthetized birds of prey by using end-tidal carbon dioxide measured with a microstream capnometer.

The relationship between end-tidal partial pressure of carbon dioxide (PETCO2), arterial partial pressure of carbon dioxide (PaCO2), and blood pH in isoflurane-anesthetized raptors was evaluated. PaCO2 and pH were determined in serial arterial samples from isoflurane anesthetized birds and compared with concurrent end-tidal partial pressure of carbon dioxide measured with a Microstream sidestream capnograph. Forty-eight paired samples, taken from 11 birds of prey (weighing 416-2,062 g), were used to determine correlations coefficients between PaCO2 and PETCO2, and between PETCO2 and pH. Limits of agreement between PaCO2 and PETCO2 also were calculated. Strong correlations were observed between PaCO2 and PETCO2 (r = 0.94; P < 0.0001) as well as between PETCO2 and pH (r = -0.90; P < 0.0001). However, the level of agreement between PaCO2 and PETCO2 varied considerably. Low values of PETCO2, ranging from 18 to 29 mm Hg, exceeded the concomitantly measured values of PaCO2 by an average of 6.0 mm Hg (6.0 +/- 1.9 mm Hg; mean +/- SD). Conversely, high values of PETCO2, ranging from 50 to 63 mm Hg, were on average 7.6 mm Hg (7.6 +/- 9.8 mm Hg) lower than values of PaCO2. In the 30 to 49 mm Hg range for PETCO2, the difference between PETCO2 and PaCO2 was on average 1.0 mm Hg (1.0 +/- 8.5 mm Hg). These results suggest that the capnograph used provided a sufficiently accurate estimation of arterial partial pressure of carbon dioxide for birds weighing > 400 g and receiving manual positive ventilation with a Bain system. In our study, the linear relationship observed between the pH and the end-tidal partial pressure of carbon dioxide suggested that the monitoring of end-tidal partial pressure of carbon dioxide also can be useful to prevent respiratory acidosis.     

Comparison of a sidestream capnograph and a mainstream capnograph in mechanically ventilated dogs

OBJECTIVE: To compare the ability of a sidestream capnograph and a mainstream capnograph to measure end-tidal CO2 (ETCO2) and provide accurate estimates of PaCO2 in mechanically ventilated dogs. DESIGN: Randomized, double Latin square. ANIMALS: 6 healthy adult dogs. PROCEDURE: Anesthesia was induced and neuromuscular blockade achieved by IV administration of pancuronium bromide. Mechanical ventilation was used to induce conditions of standard ventilation, hyperventilation, and hypoventilation. While tidal volume was held constant, changes in minute volume ventilation and PaCO2 were made by changing the respiratory rate. Arterial blood gas analysis was performed and ETCO2 measurements were obtained by use of either a mainstream or a sidestream capnographic analyzer. RESULTS: A linear regression model and bias analysis were used to compare PaCO2 and ETCO2 measurements; ETCO2 measurements obtained by both capnographs correlated well with PaCO2. Compared with PaCO2, mainstream ETCO2 values differed by 3.15 +/- 4.89 mm Hg (mean bias +/- SD), whereas the bias observed with the sidestream ETCO2 system was significantly higher (5.65 +/- 5.57 mm Hg). Regardless of the device used to measure ETCO2, bias increased as PaCO2 exceeded 60 mm Hg. CONCLUSIONS AND CLINICAL RELEVANCE: RelevancehAlthough the mainstream cas slightly more accurate, both methods of ETCO2 measurement correlated well with PaCO2 and reflected changes in the ventilatory status. However, ETCO2 values > 45 mm Hg may inaccurately reflect the severity of hypoventilation as PaCO2 may be underestimated during conditions of hypercapnia (PaCO2 > 60 mm Hg).     

Arrhythmogenic effect of hypercapnia in ducks anesthetized with halothane

OBJECTIVE: To determine effects of hypercapnia on arrhythmias in ducks anesthetized with halothane. ANIMALS: 12 ducks, 6 to 8 months old, weighing 1.1 to 1.6 kg. PROCEDURES: Each duck was anesthetized with a 1.5% mixture of halothane in oxygen, and anesthetic depth was stabilized during a 20-minute period. We added CO2 to the inspired oxygen to produce CO2 partial pressures of 40, 60, and 80 mm Hg in the inspired gas mixture.The CO2 partial pressure was increased in a stepwise manner. When arrhythmias were not evident during inhalation of the gas mixture at a specific CO2 partial pressure, the CO2 partial pressure was maintained for 10 minutes before a sample was collected for blood gas analysis. When arrhythmias were detected, a sample for blood gas analysis was collected after the CO2 partial pressure was maintained for at least 2 minutes, and CO2 inhalation then was terminated. RESULTS: During the stabilization period, PaCO2 (mean +/- SD) was 33 +/- 5 mm Hg,and arrhythmias were not detected. In 6 ducks, arrhythmias such as unifocal and multifocal premature ventricular contractions developed during inhalation of CO2. Mean PaCO2 at which arrhythmias developed was 67 +/- 12 mm Hg. In 5 of 6 ducks with arrhythmias, the arrhythmias disappeared after CO2 inhalation was terminated. CONCLUSION AND CLINICAL RELEVANCE: Analysis of data from this study indicated that hypercapnia can lead to arrhythmias in ducks during halothane-induced anesthesia. Thus, ventilatory support to maintain normocapnia is important for managing ducks anesthetized with halothane.     

Severe hypoxaemia in field-anaesthetised white rhinoceros (Ceratotherium simum) and effects of using tracheal insufflation of oxygen

White rhinoceros anaesthetised with etorphine and azaperone combination develop adverse physiological changes including hypoxia, hypercapnia, acidosis, tachycardia and hypertension. These changes are more marked in field-anaesthetised rhinoceros. This study was designed to develop a technique to improve safety for field-anaesthetised white rhinoceros by tracheal intubation and oxygen insufflation. Twenty-five free-ranging white rhinoceros were anaesthetised with an etorphine and azaperone combination for translocation or placing microchips in their horns. Once anaesthetised the rhinoceros were monitored prior to crating for transportation or during microchip placement. Physiological measurements included heart and respiratory rate, blood pressure and arterial blood gas samples. Eighteen rhinoceros were intubated using an equine nasogastric tube passed nasally into the trachea and monitored before and after tracheal insufflation with oxygen. Seven rhinoceros were not intubated or insufflated with oxygen and served as controls. All anaesthetised rhinoceros were initially hypoxaemic (percentage arterial haemoglobin oxygen saturation (%O2Sa) = 49% +/- 16 (mean +/- SD) and PaO2 = 4.666 +/- 1.200 kPa (35 +/- 9 mm Hg)), hypercapnic (PaCO2 = 8.265 +/- 1.600 kPa (62 +/- 12 mm Hg)) and acidaemic (pHa = 7.171 +/- 0.073 ). Base excess was -6.7 +/- 3.9 mmol/l, indicating a mild to moderate metabolic acidosis. The rhinoceros were also hypertensive (systolic blood pressure = 21.861 +/- 5.465 kPa (164 +/- 41 mm Hg)) and tachycardic (HR = 107 +/- 31/min). Following nasal tracheal intubation and insufflation, the %O2Sa and PaO2 increased while blood pHa and PaCO2 remained unchanged. Tracheal intubation via the nose is not difficult, and when oxygen is insufflated, the PaO2 and the %O2Sa increases, markedly improving the safety of anaesthesia, but this technique does not correct the hypercapnoea or acidosis. After regaining their feet following reversal of the anaesthesia, the animals' blood gas values return towards normality.     

Modification of cardiopulmonary and intestinal motility effects of xylazine with glycopyrrolate in horses.

Xylazine (XYL) administration in horses is accompanied by significant cardiovascular depression characterized by a 25-35% decrease in cardiac output (CO) which is likely to compromise tissue oxygen delivery (DO2), and usually vagally mediated bradycardia is an important cause of this reduced cardiovascular performance. To examine the possible benefit of preventing the bradycardiac response, 6 healthy horses were treated with intravenous (IV) saline (SAL) or 2.5 micrograms/kg glycopyrrolate (GLY) in a blinded, randomized, crossover trial. Fifteen minutes later, 1 mg/kg XYL was administered IV and systolic, diastolic and mean blood pressures (SBP, DBP, and MBP, respectively), central venous pressure (CVP), mean pulmonary artery pressure, heart rate (HR), CO, and arterial and mixed venous blood gases were measured at the following times: baseline, 2, 5, and 10 min post-SAL or GLY; and 2, 5, 10, 15, 30, 45 and 60 min post-XYL. Determination of cardiac index (CI), stroke index (SI), left ventricular work, systemic vascular resistance (SVR), DO2, oxygen uptake, and oxygen extraction ratio were made at the same time. Gastrointestinal (GI) motility was evaluated by four-quadrant auscultation for 24 h post-XYL. Statistical analysis of continuous variables was carried out using ANOVA for repeated measures and Wilcoxon's rank-sum test for non-parametric data. In GLY treated horses, HR, SBP, MBP, DBP, CI, DO2 and mixed venous oxygen tension were significantly higher up to 30 min after XYL (P < or = 0.02) while CVP and SI were significantly lower 2 and 5 min post-XYL, respectively. In both groups, GI motility as assessed by auscultation was virtually abolished for an hour, with a non-significant tendency for the decrease in motility to last longer in the GLY/XYL group. None of the treated horses developed abdominal discomfort. No significant difference was observed in the other variables. The study shows that 2.5 micrograms/kg GLY premedication reduces the cardiovascular depression caused by 1 mg/kg XYL, without adversely affecting GI motility.     

Detomidine-Propofol Anesthesia for Abdominal Surgery in Horses

OBJECTIVE: To evaluate propofol for induction and maintenance of anesthesia, after detomidine premedication, in horses undergoing abdominal surgery for creation of an experimental intestinal adhesion model. STUDY DESIGN: Prospective study. ANIMALS: Twelve horses (424 +/- 81 kg) from 1 to 20 years of age (5 females, 7 males). METHODS: Horses were premedicated with detomidine (0.015 mg/kg i.v.) 20 to 25 minutes before induction, and a propofol bolus (2 mg/kg i.v.) was administered for induction. Propofol infusion (0.2 mg/kg/min i.v.) was used to maintain anesthesia. The infusion rate was adjusted to maintain an acceptable anesthetic plane as determined by muscle relaxation, occular signs, response to surgery, and cardiopulmonary responses. Oxygen (15 L/min) was insufflated through an endotracheal tube as necessary to maintain the SpO2 greater than 90%. Systolic (SAP), mean (MAP), and diastolic (DAP) arterial pressures, heart rate (HR), electrocardiogram (ECG), respiratory rate (RR), SpO2 (via pulse oximetry), and nasal temperature were recorded at 15 minute intervals, before premedication and after induction of anesthesia. Arterial blood gas samples were collected at the same times. Objective data are reported as mean (+/-SD); subjective data are reported as medians (range). RESULTS: Propofol (2.0 mg/kg i.v.) induced anesthesia (mean bolus time, 85 sec) within 24 sec (+/-22 sec) after the bolus was completed. Induction was good in 10 horses; 2 horses showed signs of excitement and these two inductions were not smooth. Propofol infusion (0.18 mg/kg/min +/- 0.04) was used to maintain anesthesia for 61 +/- 19 minutes with the horses in dorsal recumbency. Mean SAP, DAP, and MAP increased significantly over time from 131 to 148, 89 to 101, and 105 to 121 mm Hg, respectively. Mean HR varied over time from 43 to 45 beats/min, whereas mean RR increased significantly over anesthesia time from 4 to 6 breaths/min. Mean arterial pH decreased from a baseline of 7.41 +/- 0.07 to 7.30 +/- 0.05 at 15 minutes of anesthesia, then increased towards baseline values. Mean PaCO2 values increased during anesthesia, ranging from 47 to 61 mm Hg whereas PaO2 values decreased from baseline (97 +/- 20 mm Hg), ranging from 42 to 57 mm Hg. Muscle relaxation was good and no horses moved during surgery: Recovery was good in 9 horses and acceptable in 3; mean recovery time was 67 +/- 29 minutes with 2.4 +/- 2.4 attempts necessary for the horses to stand. CONCLUSIONS: Detomidine-propofol anesthesia in horses in dorsal recumbency was associated with little cardiovascular depression, but hypoxemia and respiratory depression occurred and some excitement was seen on induction. CLINICAL RELEVANCE: Detomidine-propofol anesthesia is not recommended for surgical procedures in horses if dorsal recumbency is necessary and supplemental oxygen is not available (eg, field anesthesia).     

Inadequacy of low-volume resuscitation with hemoglobin-based oxygen carrier hemoglobin glutamer-200 (bovine) in canine hypovolemia

Stroma-free hemoglobin-based oxygen carriers (HBOC) have been developed to overcome problems associated with transfusion of allogeneic blood. We have studied the efficacy of the first licensed veterinary blood substitute, hemoglobin glutamer-200 bovine (Oxyglobin; Biopure, Cambridge, MA, USA, Hb-200), in a canine model of acute hypovolemia and examined whether clinically commonly used criteria are adequate to guide fluid resuscitation with this product. Twelve anesthetized dogs were instrumented for measurements of physiological variables including hemodynamic, oxygenation, and blood gas and acid-base parameters. Dogs were bled to a mean arterial pressure (MAP) of 50 mmHg for 1 h followed by resuscitation with either shed blood (controls) or Hb-200 until heart rate (HR), MAP and central venous pressure (CVP) returned to baseline. Recordings were repeated immediately and 3 h after termination of fluid resuscitation. Hemorrhage (average 32 mL/kg) caused significant decreases in total hemoglobin (Hb), mean pulmonary arterial pressure (PAP), cardiac output (CO) and oxygen delivery (DO2I), increases in HR and systemic vascular resistance (SVRI), and lactic acidosis. In controls, only re-transfusion of all shed blood returned HR, MAP and CVP to prehemorrhage values, whereas in other dogs this endpoint was reached with infusion of 10 mL/kg Hb-200. Unlike blood transfusion, Hb-200 infusion failed to return CI and DO2I to baseline and to increase arterial oxygen content (CaO2) and total Hb; SVRI further increased. Thus, commonly used criteria (HR, MAP, CVP) to guide transfusion therapy in patients posthemorrhage prove insufficient when HBOCs with pronounced vasoconstrictive action are used and lead to inadequate volume repletion.     

Evaluation of a combined transcutaneous carbon dioxide pressure and pulse oximetry sensor in adult sheep and dogs

OBJECTIVE: To evaluate a combined transcutaneous carbon dioxide pressure (tcPCO(2)) and pulse oximetry sensor in sheep and dogs. ANIMALS: 13 adult sheep and 11 adult dogs. PROCEDURES: During inhalation anesthesia, for the first 10 minutes following sensor placement, arterial blood gas was analyzed and tcPCO(2) was recorded every 2 minutes. Subsequently, the animals were hyper-, normo-, and hypoventilated. The simultaneously obtained tcPCO(2) and PaCO(2) values were analyzed by use of Bland-Altman statistical analysis. RESULTS: Mean +/- SD overall difference between tcPCO(2) and PaCO(2) 10 minutes after sensor application was 13.3 +/- 8.4 mm Hg in sheep and 8.9 +/- 12 mm Hg in dogs. During hyper-, normo-, and hypoventilation, mean difference (bias) and precision (limits of agreement [bias +/- 2 SD]) between tcPCO(2) and PaCO(2) values were 13.2 +/- 10.4 mm Hg (limits of agreement, -7.1 and 33.5 mm Hg) in sheep and 10.6 +/- 10.5 mm Hg (limits of agreement, -9.9 and 31.2 mm Hg) in dogs, respectively. Changes in PaCO(2) induced by different ventilation settings were detected by the tcPCO(2) sensor with a lag (response) time of 4.9 +/- 3.5 minutes for sheep and 6.2 +/- 3.6 minutes for dogs. CONCLUSIONS AND CLINICAL RELEVANCE: The tcPCO(2) sensor overestimated PaCO(2) in sheep and dogs and followed changes in PaCO(2) with a considerable lag time. The tcPCO(2) sensor might be useful for noninvasive monitoring of changes but cannot be used as a surrogate measure for PaCO(2).     

Assessment of isoflurane-induced anesthesia in ferrets and rats

OBJECTIVE: To characterize isoflurane (ISO)-induced anesthesia in ferrets and rats. ANIMALS: 8 ferrets (Mustela putorius furo) and 8 Sprague-Dawley rats. PROCEDURE: Ferrets and rats were anesthetized in a similar manner, using ISO in oxygen. Minimum alveolar concentration (MAC) was determined, using the tail-clamp method. Immediately thereafter, assessments were recorded for 0.8, 1.0, 1.5, and 2.0 MAC (order randomized) of ISO. RESULTS: MAC of ISO was (mean +/- SEM) 1.74 +/- 0.03 and 1.58 +/- 0.05% for ferrets and rats, respectively. Mean arterial blood pressure (MAP) was 75.0 +/- 4.3 and 107.9 +/- 2.7 mm Hg at 0.8 MAC for ferrets and rats, respectively, and decreased in a parallel dose-dependent manner. Respiratory frequency decreased in rats as ISO dose increased; however, respiratory frequency increased in ferrets as ISO dose increased from 0.8 to 1.5 MAC but then decreased at 2.0 MAC. At 0.8 MAC, hypoventilation was much greater in ferrets (PaCO2 = 71.4 +/- 3.5 mm Hg), compared with rats (PaCO2 = 57.7 +/- 1.9 mm Hg). In both species, PaCO2 progressively increased as anesthetic dose increased. Eyelid aperture of ferrets increased in a dose-dependent manner. Pupil diameter in ferrets and rats increased as ISO dose increased. CONCLUSIONS AND CLINICAL RELEVANCE: The MAP and PaCO2 in ferrets and rats and eyelid aperture in ferrets consistently and predictably changed in response to changes in anesthetic dose of ISO. Magnitude of respiratory depression was greater in ferrets than rats. Changes in MAP and PaCO2 in ferrets and rats and eyelid aperture in ferrets are consistent guides to changes in depth of ISO-induced anesthesia.     

Interand Intraindividual Variation in Doppler Ultrasonic Indirect Blood Pressure Measurements in Healthy Cats

This study was undertaken to evaluate reference ranges for systolic blood pressure (SBP) in cats under conditions mimicking a clinical setting. SBP was measured in 50 healthy adult cats of various ages (range, 1.5-16 years) and body weights (range, 2.2-6.1 kg) by Doppler ultrasonic sphygmomanometry. A cuff width of 2.5 cm was used, placed on the left antebrachium, and this represented a mean cuff width of 35% limb circumference (range, 31-42%). The mean (+/-SD) SBP in the 50 cats was 162 +/- 19 mm Hg (range 124-210), with only 1 cat having a SBP > or = 200 mm Hg. No significant difference (P > .05) in SBP was found between male and female cats, and no significant correlation was found between SBP and age (r(s) = 0.075) or body weight (r(s) = 0.007). Further studies in some of these cats indicated that allowing a period of 10 minutes for acclimatization to the environment where SBP was recorded resulted in a significant decrease in SBP from 176 +/- 17 to 157 +/- 21 mm Hg (n = 7) and that use of a 3.3-cm-width cuff resulted in a significant decrease in measured SBP from 168 +/- 13 to 164 +/- 13 mm Hg (n = 10). Reproducibility of SBP measurements was evaluated in 7 cats by assessing SBP 7 times at intervals of > or = 24 hours over a 10-day period. These 7 cats had a low intraindividual coefficient of variation of SBP measurements (CV < or = 7.9%) although 2 of the 7 cats had SBP values > 200 mm Hg on at least 1 occasion.     

Effects of xylazine on ventilation in horses.

The effects of 3 commonly used dosages (0.3, 0.5, and 1.1 mg/kg of body weight, IV) of xylazine on ventilatory function were evaluated in 6 Thoroughbred geldings. Altered respiratory patterns developed with all doses of xylazine, and horses had apneic periods lasting 7 to 70 seconds at the 1.1 mg/kg dosage. Respiratory rate, minute volume, and partial pressure of oxygen in arterial blood (PaO2) decreased significantly (P less than 0.001) with time after administration of xylazine, but significant differences were not detected among dosages. After an initial insignificant decrease at 1 minute after injection, tidal volume progressively increased and at 5 minutes after injection, tidal volume was significantly (P less than 0.01) greater than values obtained before injection. Partial pressure of carbon dioxide in arterial blood (PaCO2) was insignificantly increased. After administration of xylazine at a dosage of 1.1 mg/kg, the mean maximal decrease in PaO2 was 28.2 +/- 8.7 mm of Hg and 22.2 +/- 4.9 mm of Hg, measured with and without a respiratory mask, respectively. Similarly, the mean maximal increase in PaCO2 was 4.5 +/- 2.3 mm of Hg and 4.2 +/- 2.4 mm of Hg, measured with and without the respiratory mask, respectively. Significant interaction between use of mask and time was not detected, although the changes in PaO2 were slightly attenuated when horses were not masked. The temporal effects of xylazine on ventilatory function in horses should be considered in selecting a sedative when ventilation is inadequate or when pulmonary function testing is to be performed.     

Reference cardiopulmonary physiologic parameters for standing, unrestrained white rhinoceroses (Ceratotherium simum).

Chemical restraint is an important tool for the management and medical care of both captive and free-ranging rhinoceroses. Current anesthetic protocols for the white rhinoceros (Ceratotherium simum) are reported to cause varying degrees of hypertension, tachycardia, muscular stiffness and fasciculation, acidosis, and, most importantly, respiratory depression with resulting hypoventilation, hypoxia, and hypercapnea. To assist in the assessment and development of new and improved anesthetic techniques for the white rhinoceros, the following cardiopulmonary reference parameters for standing, unrestrained white rhinoceroses were generated (mean +/- standard error [minimum maximum]): heart rate = 39 +/- 0.8 beats/min (32-42), respiratory rate = 19 +/- 0.6 breaths/min (16-23), corrected indirect systolic blood pressure = 160 +/- 2.9 mm Hg (146-183), corrected indirect diastolic blood pressure = 104 +/- 2.3 mm Hg (88-117), corrected indirect mean blood pressure = 124 +/- 2.2 mm Hg (108-135), end tidal CO2 = 45.1 +/- 0.7 mm Hg (41.7-48.0), rectal temperature = 36.8 +/- 0.1 degrees C (36.6-37.2), arterial blood pH = 7.391 +/- 0.007 (7.346-7.431), arterial partial pressure of oxygen = 98.2 +/- 1.4 mm Hg (90.2-108.6), arterial partial pressure of CO2 = 49.0 +/- 0.9 mm Hg (44.4-53.7), base excess = 3.5 +/- 0.4 mmol/L (1.9-5.9), bicarbonate = 29.3 +/- 0.4 mmol/L (27.3-32.2), and arterial hemoglobin oxygen saturation (SaO2) = 97.2 +/- 0.1% (96.6-98.0).     

Use of end-tidal partial pressure of carbon dioxide to predict arterial partial pressure of carbon dioxide in harp seals during isoflurane-induced anesthesia

OBJECTIVE: To evaluate the relationship between end-tidal partial pressure of CO(2) (ETCO(2)) and PaCO(2) in isoflurane-anesthetized harp seals. ANIMALS: Three 5-month-old 25- to 47-kg harp seals (Phoca groenlandica). PROCEDURES: PaCO(2) was determined in serial arterial samples from isoflurane-anesthetized seals and compared with concomitant ETCO(2) measured with a side-stream microstream capnograph. Twenty-four paired samples were subjected to linear regression analysis and the Bland-Altman method for assessment of clinical suitability of the 2 methods (ie, PaCO(2) and ETCO(2) determinations). The influence of ventilation rate per minute (VR) on the ETCO(2) to PaCO(2) difference (P[ET-a] CO(2)) was examined graphically. RESULTS: The correlation coefficient between the 2 measurements was 0.94. The level of agreement between ETCO(2) and PaCO(2) varied considerably. Values of ETCO(2) obtained with a VR of < 5 underestimated PaCO(2) to a greater degree (mean bias, -4.01 mm Hg) and had wider limits of agreement of -13.10 to 5.07 mm Hg (-4.01 mm Hg +/- 1.96 SD), compared with a VR of > or = 5 (mean bias, -2.24 mm Hg; limits of agreement, -7.79 to 3.30 mm Hg). CONCLUSIONS AND CLINICAL RELEVANCE: These results indicate that a microstream sidestream capnograph provides a noninvasive, sufficiently accurate estimation of PaCO(2) with intermittent positive ventilation at a VR > or = 5 in anesthetized harp seals.     

Surface oximetry of healthy and ischemic equine intestine

Measurements of jejunal, ileal, and large colon (pelvic flexure) surface O2 tension (PSO2) were made in halothane-anesthetized horses with a nonheated miniature oxygen polarographic electrode. Assisted ventilation with 100% O2 was used to maintain PaCO2 tension at 50 +/- 8 mm of Hg while mean arterial blood pressure was maintained greater than or equal to 70 mm of Hg. Mean +/- SD PSO2 for the intestinal segments were: jejunum (horses 1 to 4), 71 +/- 20 mm of Hg; ileum (horses 1 to 4), 61 +/- 8 mm of Hg; and pelvic flexure of the large colon (horses 1 to 10), 55 +/- 13 mm of Hg. The response of the sensor to intestinal ischemia was studied in the large colon of an additional 12 halothane-anesthetized horses, using 4 types of vascular occlusion: venous (4 horses); arterial and venous (4 horses); venous and intramural vascular obstruction (2 horses); and arterial, venous, and intramural obstruction (2 horses). Venous and arterial occlusions were maintained for 30, 60, 90, and 120 minutes, whereas intramural obstruction combined with either type of vascular obstruction was studied for 60 to 120 minutes. After vascular occlusion, PSO2 decreased to 8 +/- 7 mm of Hg for venous obstruction, 4 +/- 3 mm of Hg for arterial and venous obstruction, 6 +/- 0 mm of Hg for intramural and venous obstruction, and 3 +/- 0 mm of Hg after intramural and arterial and venous obstruction. Thirty minutes after release of the clamps, the PSO2 increased to greater than or equal to 50% of the preoccluded large colon value.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of renal insufficiency on the pharmacokinetics and pharmacodynamics of benazepril in cats

The effect of renal insufficiency was studied on the pharmacokinetics (PK) and pharmacodynamics (PD) of the angiotensin-converting enzyme (ACE) inhibitor benazepril in cats. The active metabolite of benazepril, benazeprilat, is eliminated principally ( approximately 85%) via biliary excretion in cats. A total of 20 control animals and 32 cats with moderate renal insufficiency induced by partial nephrectomy were used. Assessments were made at steady state after treatment with placebo or benazepril (0.25-2 mg/kg) once daily for a minimum of 10 days. The PK endpoint was the AUC (0-->24 h) of total plasma benazeprilat. The PD endpoints were systolic, diastolic and mean blood pressures (respectively SBP, DBP and MBP) measured by telemetry, and plasma ACE activity, assessed by an ex vivo assay. Renal function was assessed by glomerular filtration rate (GFR), measured by inulin clearance, and plasma creatinine concentrations (1/PCr). As compared with control animals, the renal insufficient cats had a 78% reduction in GFR (0.57 +/- 0.41 mL/min kg), increased plasma creatinine (2.7 +/- 1.0 mg/dL), urea (44.0 +/- 11.9 mg/dL) and ACE activity, and moderately increased blood pressure (SBP 171.8 +/- 5.1 mmHg) (all parameters P < 0.05). Renal insufficient cats receiving benazepril had significantly (P < 0.05) lower SBP, DBP, MBP and ACE, and higher GFR values as compared with placebo-treated animals. There were no significant differences in SBP, DBP, MBP, benazeprilat or ACE values according to the degree of renal insufficiency in cats receiving benazepril. It is concluded that no dose adjustment of benazepril is necessary in cats with moderate renal insufficiency.     

Effects of isovolemic resuscitation with hemoglobin-based oxygen carrier Hemoglobin glutamer-200 (bovine) on systemic and mesenteric perfusion and oxygenation in a canine model of hemorrhagic shock: a comparison with 6% hetastarch solution and shed blood

OBJECTIVE: To study Hemoglobin glutamer-200 bovine (Hb-200), 6% hetastarch (HES) and shed whole blood (WB) resuscitation in canine hemorrhagic shock. STUDY DESIGN: Prospective laboratory investigation. Animals Twelve adult dogs [29 +/- 1 kg (mean +/- SD)]. METHODS: Anesthetized dogs were instrumented for recording systemic and mesenteric hemodynamic parameters and withdrawal of arterial, mixed and mesenteric venous blood, in which hematological, oxygenation, blood gas and acid-bases variables were determined. Recordings were made before [baseline (BL)], after 1 hour of hypovolemia and immediately and 3 hours post-resuscitation with 30 mL kg(-1) of either Hb-200, HES, or WB. RESULTS: Blood withdrawal (average 34 +/- 2 mL kg(-1)) caused significant hemodynamic changes, metabolic acidosis and hyperlactatemia characteristic for hemorrhagic shock. Only WB transfusion restored all variables. Hemoglobin glutamer-200 bovine infusion returned most hemodynamic parameters including cardiac output and mesenteric arterial blood flow to BL but increased mean arterial pressure above BL (p < 0.05). However, Hb-200 failed to restore total Hb and arterial oxygen content (CaO2), leaving systemic (DO2I) and mesenteric O2 delivery (DO2Im) below BL (p < 0.05). Nevertheless, acid-base variables recovered completely after Hb-200 resuscitation, and met-hemoglobin (Met-Hb) levels increased (p < 0.05). Hetastarch resuscitation returned hemodynamic variables to or above BL but further decreased total Hb and CaO2, preventing recovery of sDO2I and mDO2I (p < 0.05). Thus, systemic and mesenteric O2 extraction stayed above BL (p < 0.05) while acid-base variables recovered to BL, although slower than in Hb-200 and WB groups (p < 0.05). CONCLUSIONS AND CLINICAL RELEVANCE: Resuscitation with Hb-200 seemed to resolve metabolic acidosis and lactatemia more rapidly than HES, but not WB; yet it is not superior to HES in improving DO2I and DO2Im. The hyperoncotic property of solutions like Hb-200 that results in rapid volume expansion with more homogenous microvascular perfusion and the ability to facilitate diffusive O2 transfer accelerating metabolic recovery may be the key mechanisms underlying their beneficial effects as resuscitants.     

Assessment of halothane and sevoflurane anesthesia in spontaneously breathing rats

OBJECTIVE: To characterize halothane and sevoflurane anesthesia in spontaneously breathing rats. ANIMALS: 16 healthy male Sprague-Dawley rats. PROCEDURE: 8 rats were anesthetized with halothane and 8 with sevoflurane. Minimum alveolar concentration (MAC) was determined. Variables were recorded at anesthetic concentrations of 0.8, 1.0, 1.25, and 1.5 times the MAC of halothane and 1.0, 1.25, 1.5, and 1.75 times the MAC of sevoflurane. RESULTS: Mean (+/- SEM) MAC for halothane was 1.02 +/- 0.02% and for sevoflurane was 2.99 +/- 0.19%. As sevoflurane dose increased from 1.0 to 1.75 MAC, mean arterial pressure (MAP) decreased from 103.1 +/- 5.3 to 67.9 +/- 4.6 mm Hg, and PaCO2 increased from 58.8 +/- 3.1 to 92.2 +/- 9.2 mm Hg. As halothane dose increased from 0.8 to 1.5 MAC, MAP decreased from 99 +/- 6.2 to 69.8 +/- 4.5 mm Hg, and PaCO2 increased from 59.1 +/- 2.1 to 75.9 +/- 5.2 mm Hg. Respiratory rate decreased in a dose-dependent fashion from 88.5 +/- 4.5 to 58.5 +/- 2.7 breaths/min during halothane anesthesia and from 42.3 +/- 1.8 to 30.5 +/- 4.5 breaths/min during sevoflurane anesthesia. Both groups of rats had an increase in eyelid and pupillary aperture with an increase in anesthetic dose. CONCLUSIONS AND CLINICAL RELEVANCE: An increase in PaCO2 and a decrease in MAP are clinical indicators of an increasing halothane and sevoflurane dose in unstimulated spontaneously breathing rats. Increases in eyelid aperture and pupil diameter are reliable signs of increasing depth of halothane and sevoflurane anesthesia. Decreasing respiratory rate is a clinical indicator of an increasing dose of halothane.     

Anesthetic and physiologic effects of tiletamine, zolazepam, ketamine, and xylazine combination (TKX) in feral cats undergoing surgical sterilization

Tiletamine (12.5 mg), zolazepam (12.5 mg), ketamine (20 mg), and xylazine (5 mg) (TKX; 0.25 ml, IM) combination was evaluated as an anesthetic in 22 male and 67 female adult feral cats undergoing sterilization at high-volume sterilization clinics. Cats were not intubated and breathed room air. Oxygen saturation (SpO(2)), mean blood pressure (MBP), heart rate (HR), respiration rate (RR), and core body temperature were recorded. Yohimbine (0.25 ml, 0.5 mg, IV) was administered at the completion of surgery. TKX produced rapid onset of lateral recumbency (4+/-1 min) and surgical anesthesia of sufficient duration to complete surgical procedures in 92% of cats. SpO(2) measured via a lingual pulse oximeter probe averaged 92+/-3% in male cats and 90+/-4% in females. SpO(2) fell below 90% at least once in most cats. MBP measured by oscillometry averaged 136+/-30 mm Hg in males and 113+/-29 mm Hg in females. MBP increased at the onset of surgical stimulation suggesting incomplete anti-nociceptive properties. HR averaged 156+/-19 bpm, and RR averaged 18+/-8 bpm. Neither parameter varied between males and females or over time. Body temperature decreased significantly over time, declining to 38.0+/-0.8 degrees C at the time of reversal in males and 36.6+/-0.8 degrees C at the time of reversal in females. Time from anesthetic reversal to sternal recumbency was prolonged (72+/-42 min). Seven cats (8%) required an additional dose of TKX to maintain an adequate plane of anesthesia at the onset of surgery, and this was associated with significantly longer recovery times (108+/-24 min).