Influence of xylazine on the function of the LiDCO sensor in isoflurane anaesthetized horses

ObjectivePrevious studies showed an influence of xylazine on the LiDCO sensor in vitro and in standing horses, but did not prove that this interaction caused error in LiDCO measurements. Therefore, agreement of cardiac output (CO) measurements by LiDCO and bolus-thermodilution (BTD) was determined in horses receiving xylazine infusions.Study designProspective, experimental study.AnimalsEight Warmblood horses.MethodsAll horses were premedicated with xylazine. Anaesthesia was induced with midazolam and ketamine and was maintained with isoflurane in oxygen. During six hours of anaesthesia CO measurements and blood samples were taken before, during and after a 60 minute period of xylazine infusion. Pairs of LiDCO and bolus thermo-dilution (BTD) measurements of CO were performed. Sensor voltages exposed to blood and saline were measured before, during and after xylazine infusion and compared using Bland-Altman method of agreement with corrections for repeated measures.ResultsThe CO values (mean ± SD) before xylazine were 34.8 ± 7.3 and 36.4 ± 8.1 L minute⁻¹ for BTD and LiDCO, respectively. After starting the xylazine infusion, the CO values for BTD decreased to 27.5 ± 6.1 L minute⁻¹ whereas CO values measured by LiDCO increased to 54.7 ± 18.4 L minute⁻¹. One hour after discontinuing xylazine infusion, CO values were 33 ± 6.7 and 36.5 ±11.9 L minute⁻¹ for BTD and LiDCO, respectively. The difference between saline and blood exposed sensor voltages decreased during xylazine infusion and these differences were positive numbers before but negative during the infusion. There were correlations between xylazine plasma concentrations, CO differences and sensor voltage differences (saline – blood).Conclusions and clinical relevanceThis study proved that xylazine infusion caused concentration dependent bias in LiDCO measurements leading to an overestimation of readings. Sensor voltage differences (saline – blood) may become valuable clinical tool to predict drug-sensor interactions.     

Effects of dobutamine on cardiovascular function and oxygen delivery in standing horses

Dobutamine is routinely used to improve cardiovascular function in anaesthetized horses. However, dobutamine in conscious horses is insufficiently investigated. Ten research horses that were already instrumented for a preceding trial were included into the study. Cardiovascular variables were recorded and blood samples taken after instrumentation (Baseline), before starting dobutamine and after 10 min of dobutamine infusion (2 µg kg⁻¹ min⁻¹). A significant increase in systemic blood pressure, mean pulmonary artery pressure and right atrial pressure, and a decrease in heart rate were observed with dobutamine compared with baseline measurements. Arterial and mixed venous haemoglobin and oxygen content, as well as mixed venous partial pressure of oxygen increased. No significant changes in cardiac output, stroke volume, systemic vascular resistance, arterial partial pressure of oxygen, or oxygen consumption, delivery and extraction ratio were detected. Concluding, dobutamine increased systemic blood pressure without detectable changes in stroke volume, cardiac output or systemic vascular resistance in conscious horses.     

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

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

Cardiovascular,respiratory, electrolyte and acid–base balance during continuous dexmedetomidine infusion in anesthetized dogs

ObjectiveTo evaluate the cardiovascular, respiratory, electrolyte and acid–base effects of a continuous infusion of dexmedetomidine during propofol–isoflurane anesthesia following premedication with dexmedetomidine.Study designProspective experimental study.AnimalsFive adult male Walker Hound dogs 1–2 years of age averaging 25.4 ± 3.6 kg.MethodsDogs were sedated with dexmedetomidine 10 μg kg^?1 IM, 78 ± 2.3 minutes (mean ± SD) before general anesthesia. Anesthesia was induced with propofol (2.5 ± 0.5 mg kg^?1) IV and maintained with 1.5% isoflurane. Thirty minutes later dexmedetomidine 0.5 μg kg^?1 IV was administered over 5 minutes followed by an infusion of 0.5 μg kg^?1 hour^?1. Cardiac output (CO), heart rate (HR), ECG, direct blood pressure, body temperature, respiratory parameters, acid–base and arterial blood gases and electrolytes were measured 30 and 60 minutes after the infusion started. Data were analyzed via multiple linear regression modeling of individual variables over time, compared to anesthetized baseline values. Data are presented as mean ± SD.ResultsNo statistical difference from baseline for any parameter was measured at any time point. Baseline CO, HR and mean arterial blood pressure (MAP) before infusion were 3.11 ± 0.9 L minute^?1, 78 ± 18 beats minute^?1 and 96 ± 10 mmHg, respectively. During infusion CO, HR and MAP were 3.20 ± 0.83 L minute^?1, 78 ± 14 beats minute^?1 and 89 ± 16 mmHg, respectively. No differences were found in respiratory rates, PaO₂, PaCO₂, pH, base excess, bicarbonate, sodium, potassium, chloride, calcium or lactate measurements before or during infusion.Conclusions and clinical relevanceDexmedetomidine infusion using a loading dose of 0.5 μg kg^?1 IV followed by a constant rate infusion of 0.5 μg kg^?1 hour^?1 does not cause any significant changes beyond those associated with an IM premedication dose of 10 μg kg^?1, in propofol–isoflurane anesthetized dogs. IM dexmedetomidine given 108 ± 2 minutes before onset of infusion showed typical significant effects on cardiovascular parameters.     

Use of lithium dilution and pulse contour analysis cardiac output determination in anaesthetized horses: a clinical evaluation

OBJECTIVE: To assess the suitability of a human algorithm for calculation of continuous cardiac output from the arterial pulse waveform, in anaesthetized horses. STUDY DESIGN: Prospective clinical study. ANIMALS: Twenty-four clinical cases undergoing anaesthesia for various conditions. MATERIALS AND METHODS: Cardiac output (Qt), measured by lithium dilution (QtLiDCO), was compared with a preceding, calibrated Qt measured from the pulse waveform (QtPulse). These comparisons were repeated every 20-30 minutes. Positive inotropes or vasopressors were administered when clinically indicated. Cardiac indices from 30.7 to 114.9 mL kg(-1) minute(-1) were recorded. Unusually shaped QtLiDCO curves were rejected and the measurement was repeated immediately. RESULTS: Eighty-nine comparisons were made between QtLiDCO and QtPulse. The bias between the mean (+/-SD) of the two methods (QtLiDCO - QtPulse) was -0.07 L minute(-1)(+/-3.08) (0.24 +/- 6.48 mL kg(-1) minute(-1)). The limits of agreement were -12.72 and 13.2 mL kg(-1) minute(-1) (Bland & Altman 1986; Mantha et al. 2000). Linear regression analysis demonstrated a correlation coefficient (r2) of 0.89. Cardiac output in individual patients varied from 49.1 to 183% of the initial measurement at the time of calibration. Linear regression of log-transformed Qt variation for each method found a mean difference of 9% with limits of agreement of -4.1 to 22.1%. CONCLUSIONS AND CLINICAL RELEVANCE: This method of pulse contour analysis is a relatively noninvasive and reliable way of monitoring continuous Qt in the horse under anaesthesia. The ability to easily monitor Qt might decrease morbidity and mortality in the anaesthetized horse.     

Cardiovascular effects of dose escalating of norepinephrine in healthy dogs anesthetized with isoflurane

ObjectiveTo evaluate the systemic cardiovascular effects of dose escalating administration of norepinephrine in healthy dogs anesthetized with isoflurane.Study designExperimental study.AnimalsA total of six adult laboratory Beagle dogs, 10.5 (9.2–12.0) kg [median (range)].MethodsEach dog was anesthetized with isoflurane at an end-tidal concentration of 1.7%, mechanically ventilated and administered a continuous rate infusion of rocuronium (0.5 mg kg^–1 hour^–1). Each dog was administered incremental dose rates of norepinephrine (0.05, 0.125, 0.25, 0.5, 1.0 and 2.0 μg kg^–1 minute^–1), and each dose was infused for 15 minutes. Cardiovascular variables were recorded before administration and at the end of each infusion period.ResultsNorepinephrine infusion increased mean arterial pressure (MAP), cardiac output (CO) and oxygen delivery in a dose-dependent manner. Systemic vascular resistance did not significantly change during the experiment. Stroke volume increased at the lower dose rates and heart rate increased at the higher dose rates. Oxygen consumption and lactate concentrations did not significantly change during infusions.ConclusionsIn dogs anesthetized with isoflurane, norepinephrine increased MAP by increasing the CO. CO increased with a change in stroke volume at lower dose rates of norepinephrine. At higher dosage, heart rate also contributed to an increase in CO. Norepinephrine did not cause excessive vasoconstriction that interfered with the CO during this study.Clinical relevanceNorepinephrine can be useful for treating hypotension in dogs anesthetized with isoflurane.     

The effects of halothane and isoflurane on cardiovascular function in dorsally recumbent horses undergoing surgery

ObjectiveTo determine the haemodynamic effects of halothane and isoflurane with spontaneous and controlled ventilation in dorsally recumbent horses undergoing elective surgery.Study designProspective randomized clinical trial.AnimalsTwenty-five adult horses, body mass 487 kg (range: 267–690).MethodsHorses undergoing elective surgery in dorsal recumbency were randomly assigned to one of four treatment groups, isoflurane (I) or halothane (H) anaesthesia, each with spontaneous (SB) or controlled ventilation (IPPV). Indices of cardiac function and femoral arterial blood flow (ABF) and resistance were measured using transoesophageal and transcutaneous Doppler echocardiography, respectively. Arterial blood pressure was measured directly.ResultsFour horses assigned to receive isoflurane and spontaneous ventilation (SBI) required IPPV, leaving only three groups for analysis: SBH, IPPVH and IPPVI. Two horses were excluded from the halothane groups because dobutamine was infused to maintain arterial blood pressure. Cardiac index (CI) was significantly greater, and pre-ejection period (PEP) shorter, during isoflurane compared with halothane anaesthesia with both spontaneous (p = 0.04, p = 0.0006, respectively) or controlled ventilation (p = 0.04, p = 0.008, respectively). There was an association between CI and PaCO₂ (p = 0.04) such that CI increased by 0.45 L minute⁻¹m⁻² for every kPa increase in PaCO₂. Femoral ABF was only significantly higher during isoflurane compared with halothane anaesthesia during IPPV (p = 0.0006). There was a significant temporal decrease in CI, but not femoral arterial flow.ConclusionThe previously reported superior cardiovascular function during isoflurane compared with halothane anaesthesia was maintained in horses undergoing surgery. However, in these clinical subjects, a progressive decrease in CI, which was independent of ventilatory mode, was observed with both anaesthetic agents.Clinical relevanceCardiovascular function may deteriorate progressively in horses anaesthetized for brief (<2 hours) surgical procedures in dorsal recumbency. Although cardiovascular function is superior with isoflurane in dorsally recumbent horses, the need for IPPV may be greater.     

Assessment of cardiac output measurement in dogs by transpulmonary pulse contour analysis

Objective – To determine if metatarsal artery pressure (COmet) is comparable to femoral artery pressure (COfem) as the input for transpulmonary pulse contour analysis (PiCCO) in anesthetized dogs, using the lithium dilution method (LiDCO) as a standard for cardiac output (CO) measurement. Design – Prospective randomized study. Setting – University research laboratory. Animals – Ten healthy purpose‐bred mixed breed dogs were anesthetized and instrumented to measure direct blood pressure, heart rate, arterial blood gases, and CO. Interventions – The CO was measured using LiDCO and PiCCO techniques. Animals had their right femoral and left distal metatarsal artery catheterized for proximal (COfem) and distal (COmet) PiCCO analysis, respectively. Measurements were obtained from each animal during low, normal, and high CO states by changing amount of inhalant anesthetics and heart rate. Measurements were converted to CO indexed to body weigh (CI_BW=CO/kg) for statistical analysis. Agreement was determined using Bland and Altman analysis and concordance correlation coefficients. Measurements and Main Results – Thirty paired measurements were taken. The LiDCO CI_BW (± SD) was 68.7 ± 30.3, 176.0 ± 53.0, and 211.1 ± 76.5 mL/kg/min during low, normal, and high CO states, respectively. There was a significant effect of CI_BW state on bias and relative bias with COmet (P<0.001 and P=0.003, respectively). Bias of the COmet method (± SD) was ?116.6 (70.5), 20.1(76.4), and 91.3 (92.0) mL/kg/min at low, normal, and high CI_BW, respectively. Bias of the COfem (± SD) was ?20.3 (19.0), 8.6 (70.9), and ?2.9 (83.0) mL/kg/min at low, normal, and high CI_BW, respectively. The mean relative bias for COfem was ?6.7 ± 44% (limits of agreements: ?81.2 to 67.9%). Conclusion – Compared with lithium dilution, the pulse contour analysis provides a good estimation of CO, but requires femoral artery catheterization in anesthetized dogs.     

Preliminary evaluation of the effects of a 1:1 inspiratory-to-expiratory ratio in anesthetized and ventilated horses

ObjectiveTo describe some cardiorespiratory effects of an inspiratory-to-expiratory (IE) ratio of 1:1 compared with 1:3 in ventilated horses in dorsal recumbency.Study designRandomized crossover experimental study.AnimalsA total of eight anesthetized horses, with 444 (330–485) kg body weight [median (range)].MethodsHorses were ventilated in dorsal recumbency with a tidal volume of 15 mL kg^–1 and a respiratory rate of 8 breaths minute^–1, and IE ratios of 1:1 (IE1:1) and 1:3 (IE1:3) in random order, each for 25 minutes after applying a recruitment maneuver. Spirometry, arterial blood gases and dobutamine requirements were recorded in all horses during each treatment. Electrical impedance tomography (EIT) data were recorded in four horses and used to generate functional EIT variables including regional ventilation delay index (RVD), a measure of speed of lung inflation, and end-expiratory lung impedance (EELI), an indicator of functional residual capacity (FRC). Results were assessed with linear and generalized linear mixed models.ResultsCompared with treatment IE1:3, horses ventilated with treatment IE1:1 had higher mean airway pressures and respiratory system compliance (p < 0.014), while peak, end-inspiratory and driving airway pressures were lower (p < 0.001). No differences in arterial oxygenation or dobutamine requirements were observed. PaCO₂ was lower in treatment IE1:1 (p = 0.039). Treatment IE1:1 resulted in lower RVD (p < 0.002) and higher EELI (p = 0.023) than treatment IE1:3.Conclusions and clinical relevanceThese results suggest that IE1:1 improved respiratory system mechanics and alveolar ventilation compared with IE1:3, whereas oxygenation and dobutamine requirements were unchanged, although differences were small. In the four horses where EIT was evaluated, IE1:1 led to a faster inflation rate of the lung, possibly the result of increased FRC. The clinical relevance of these findings needs to be further investigated.     

Dose-dependent effects of isoflurane and dobutamine on cardiovascular function in dogs with experimental mitral regurgitation

Objective

To investigate the dose-dependent effects of isoflurane and dobutamine on haemodynamics in dogs with experimentally induced mitral valve insufficiency (MI).

Influence of a constant rate infusion of dexmedetomidine on cardiopulmonary function and recovery quality in isoflurane anaesthetized horses

ObjectiveTo investigate the influence of a dexmedetomidine constant rate infusion (CRI) in horses anaesthetized with isoflurane.Study designProspective, randomized, blinded, clinical study.AnimalsForty adult healthy horses (weight mean 491 ± SD 102 kg) undergoing elective surgery.MethodsAfter sedation [dexmedetomidine, 3.5 μg kg^?1 intravenously (IV)] and induction IV (midazolam 0.06 mg kg^?1, ketamine 2.2 mg kg^?1), anaesthesia was maintained with isoflurane in oxygen/air (FiO₂ 55–60%). Horses were ventilated and dobutamine was administered when hypoventilation [arterial partial pressure of CO₂ > 8.00 kPa (60 mmHg)] and hypotension [arterial pressure 70 mmHg] occurred respectively. During anaesthesia, horses were randomly allocated to receive a CRI of dexmedetomidine (1.75 μg kg^?1 hour^?1) (D) or saline (S). Monitoring included end-tidal isoflurane concentration, cardiopulmonary parameters, and need for dobutamine and additional ketamine. All horses received 0.875 μg kg^?1 dexmedetomidine IV for the recovery period. Age and weight of the horses, duration of anaesthesia, additional ketamine and dobutamine, cardiopulmonary data (anova), recovery scores (Wilcoxon Rank Sum Test), duration of recovery (t-test) and attempts to stand (Mann–Whitney test) were compared between groups. Significance was set at p < 0.05.ResultsHeart rate and arterial partial pressure of oxygen were significantly lower in group D compared to group S. An interaction between treatment and time was present for cardiac index, oxygen delivery index and systemic vascular resistance. End-tidal isoflurane concentration and heart rate significantly increased over time. Packed cell volume, systolic, diastolic and mean arterial pressure, arterial oxygen content, stroke volume index and systemic vascular resistance significantly decreased over time. Recovery scores were significantly better in group D, with fewer attempts to stand and significantly longer times to sternal position and first attempt to stand.Conclusions and clinical relevance A dexmedetomidine CRI produced limited cardiopulmonary effects, but significantly improved recovery quality.     

Agreement of high definition oscillometry with direct arterial blood pressure measurement at different blood pressure ranges in horses under general anaesthesia

ObjectiveTo determine the agreement of high definition oscillometry (HDO) with direct arterial blood pressure measurements in normotensive, hypotensive and hypertensive horses during general anaesthesia.Study designExperimental study.AnimalsSeven healthy warmblood horses, aged 3–11 years, weighing 470–565 kg.MethodsMeasurements from a HDO device with the cuff placed around the base of the tail were compared with pressures measured invasively from the facial artery. High blood pressures were induced by intravenous (IV) administration of dobutamine (5 μg kg⁻¹ minute⁻¹) over ten minutes followed by norepinephrine (0.1 mg kg⁻¹ IV) and low pressures by increasing the inspired fraction of isoflurane and administration of nitroglycerine (0.05 mg kg⁻¹ IV). For analysis three pressure levels were determined: high (MAP>110 mmHg), normal (60 mmHgResultsA total of 245 paired measurements of systolic (SAP), mean (MAP) and diastolic (DAP) pressures were obtained. The HDO device underestimated blood pressure at hypertensive and normotensive levels and overestimated blood pressure at hypotensive levels. Best agreement was obtained for SAP and MAP within normotensive limits. At normotension, bias ± standard deviation for SAP, MAP and DAP were 0.1 ± 19.4 mmHg, 0.5 ± 14.0, 4.7 ± 15.6, respectively. At high pressure levels bias and SD were 26.1 ± 37.3 (SAP), 4.2 ± 19.4 (MAP), 1.5 ± 16.8 (DAP) and at low pressures -20.0 ± 20.9 (SAP), -11.4 ± 19.6 (MAP), -4.7 ± 20.1 (DAP), with HDO measurements at a MAP <50 mmHg often failing.Conclusion and clinical relevanceGood agreement with invasive arterial blood pressures was obtained with HDO at normotensive levels in horses. At high and low pressure ranges HDO was unreliable. Therefore, if haemodynamic instability is expected, invasive measurement remains preferable.     

Preliminary study on the effects of pergolide on left ventricular function in the horses with pituitary pars intermedia dysfunction

BackgroundPituitary pars intermedia dysfunction (PPID), a neurodegenerative disease leading to reduced dopamine production, is a common disease in aged horses. The treatment is based on administration of the dopamine agonist pergolide. This drug has been related to valvular fibrosis in humans, but the cardiovascular effect of this drug has not yet been investigated in horses.ObjectivesTo determine whether pergolide induces valvular disease in horses or affects the cardiac function.MethodsStandard, tissue Doppler (TDE) and two-dimensional speckle tracking (STE) echocardiography were performed in horses with diagnosed PPID based on adrenocorticotropic hormone dosage. Measurements taken in horses treated with pergolide were compared with those from untreated horses with nonparametric t-tests. Furthermore, measurements from follow-up examinations performed at least three months after the initial exam were compared with a Wilcoxon signed rank test for repeated measurements in each group.ResultsTwenty-three horses were included. None of the 12 horses under treatment developed valvular regurgitation. Furthermore, no differences in the measurements of the left ventricular systolic or diastolic function could be seen between the group of horses with treatment and those without treatment. Measurements taken in the follow-up exam did not differ compared to those taken in the initial exam in both groups.ConclusionsNo changes of the left ventricular function assessed by TDE and STE could be shown in a small population of horses with confirmed PPID. Treatment with pergolide did not affect the ventricular function nor induce valvular disease.     

Effects of intravenous butorphanol on cardiopulmonary function in isoflurane-anesthetized alpacas

OBJECTIVE: To determine the effects of intravenous (IV) butorphanol on the cardiopulmonary system and on the bispectral index (BIS) in isoflurane-anesthetized alpacas. STUDY DESIGN: Randomized, blinded cross-over experimental trial. ANIMALS: Eight healthy, young (3 +/- 1 SD years) adult female alpacas weighing 64 +/- 9 SD kg. METHODS: Alpacas were anesthetized with isoflurane by mask followed by tracheal intubation and maintenance of anesthesia with isoflurane in oxygen and intermittent positive pressure ventilation. Animals were assigned to two treatments, butorphanol (0.1 mg kg(-1), IV) and saline (0.01 mL kg(-1), IV) in a randomized manner allowing a 2-week interval between treatments. Cardiovascular variables included systolic, diastolic, and mean arterial blood pressure, heart rate, pulmonary arterial pressure, pulmonary arterial occlusion pressure (PAOP), central venous pressure, cardiac output, and pulmonary temperature (TEMP). Cardiac index, systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR) were calculated. Bispectral index was also measured. Arterial and mixed venous blood samples were collected for blood gas analysis. All variables were recorded at baseline (time 0) and at 5, 10, 15, 30, 45 and 60 minutes following injection and were analyzed by using repeated-measures ANOVA (p < 0.05). PAOP, PVR, and BIS were analyzed by paired t-tests. RESULTS: Butorphanol decreased SVR at all times when compared with the baseline, but no difference was detected between treatments. TEMP decreased with time in both treatments, but they were not different from each other. Other cardiovascular, BIS, and blood gas variables were not different between groups. CONCLUSION AND CLINICAL RELEVANCE: We conclude that butorphanol had minimal effects on the cardiovascular system of the alpacas, causing a mild decrease in SVR.