Cardiac troponin I in dogs anaesthetized with propofol and sevoflurane: the influence of medetomidine premedication and inspired oxygen fraction

Objective

To investigate changes in serum cardiac troponin I (cTnI) concentrations in dogs in which medetomidine was used for sedation or for premedication prior to anaesthesia with propofol and sevoflurane.

Cardiac troponin I is elevated in dogs and cats with azotaemia renal failure and in dogs with non-cardiac systemic disease

OBJECTIVE: To determine if dogs and cats with renal failure, or other severe non-cardiac disease, and no antemortem evidence of cardiac disease on basic clinical evaluation, have elevated levels of cardiac troponin I (cTnI). DESIGN: Cross-sectional study using 56 dogs and 14 cats with primary non-cardiac disease (39 dogs with azotaemic renal failure, 14 cats with azotaemic renal failure, 17 dogs with non-cardiac systemic disease); 7/25 dogs and 6/14 cats had murmurs detected on physical examination. Serum or heparinised plasma was collected and analysed for cTnI. RESULTS: Cardiac troponin I concentrations were elevated above reference intervals in 70% of dogs and 70% of cats with azotaemic renal failure and in 70% of dogs with a variety of systemic non-cardiac diseases. Cardiac troponin I concentrations did not correlate with the degree of azotaemia, presence of murmurs, hypertension or type of non-cardiac illness. CONCLUSIONS: Cardiac troponin I concentration is often elevated in dogs and cats with azotaemic renal failure and in dogs with other systemic non-cardiac illness, suggesting that these conditions often result in clinically inapparent myocardial injury or possibly altered elimination of cTnI.     

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

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

RESEARCH PAPER: Comparison between two methods for cardiac output measurement in propofol‐anesthetized dogs: thermodilution and Doppler

ObjectiveTo compare cardiac output (CO) measured by Doppler echocardiography and thermodilution techniques in spontaneously breathing dogs during continuous infusion of propofol. To do so, CO was obtained using the thermodilution method (CO_TD) and Doppler evaluation of pulmonary flow (CO_DP) and aortic flow (CO_DA).Study designProspective cohort study.AnimalsEight adult dogs weighing 8.3 ± 2.0 kg.MethodsPropofol was used for induction (7.5 ± 1.9 mg kg^?1 IV) followed by a continuous rate infusion at 0.7 mg kg^?1 minute^?1. The animals were positioned in left lateral recumbency on an echocardiography table that allowed for positioning of the transducer at the 3rd and 5th intercostal spaces of the left hemithorax for Doppler evaluation of pulmonary and aortic valves, respectively. CO_DP and CO_DA were calculated from pulmonary and aortic velocity spectra, respectively. A pulmonary artery catheter was inserted via the jugular vein and positioned inside the lumen of the pulmonary artery in order to evaluate CO_TD. The first measurement of CO_TD, CO_DP and CO_DA was performed 30 minutes after beginning continuous infusion (T0) and then at 15‐minute intervals (T15, T30, T45 and T60). Numeric data were submitted to two‐way anova for repeated measurements, Pearson’s correlation coefficient and Bland &; Altman analysis. Data are presented as mean ± SD.ResultsAt T0, CO_TD was lower than CO_DA. CO_DA was higher than CO_TD and CO_DP at T30, T45 and T60. The difference between the CO_TD and CO_DP, when all data were included, was ?0.04 ± 0.22 L minute^?1 and Pearson’s correlation coefficient (r) was 0.86. The difference between the CO_TD and CO_DA was ?0.87 ± 0.54 L minute^?1 and r = 0.69. For CO_TD and CO_DP, the difference was ?0.82 ± 0.59 L minute^?1 and r = 0.61.ConclusionDoppler evaluation of pulmonary flow was a clinically acceptable method for assessing the CO in propofol‐anesthetized dogs.     

Resting concentrations of cardiac troponin I in fit horses and effect of racing

ObjectivesTo determine normal resting values for cardiac troponin I (cTnI) in healthy Standardbred, Thoroughbred and Warmblood horses and investigate if racing has an influence on cTnI concentrations.BackgroundMeasuring cTnI concentrations in plasma is the gold standard for detecting myocardial injury in humans. Cardiac troponin I is highly conserved between species and has gained interest as a marker for cardiac injury in horses. Increased levels of cTnI have been reported in association with endurance and short-term strenuous exercise on a treadmill in horses. However, the effect of true racing conditions has not yet been reported.Animals, materials and methodsBlood samples for analysis of cTnI concentrations in plasma were collected from 67 Standardbred racehorses, 34 Thoroughbred racehorses and 35 Warmblood dressage horses at rest. Blood samples were also collected prior to and after racing in 22 Standardbred racehorses and 6 Thoroughbred racehorses.ResultsAll horses except one had resting plasma cTnI concentrations <0.022 μg/L. Mild increases in cTnI concentrations were seen in some horses 1–2 h after the race (1/17 Standardbreds and 2/6 Thoroughbreds) as well as 10–14 h after the race (4/21 Standardbreds and 1/6 Thoroughbreds).ConclusionsResting cTnI concentrations in horses are low but mildly elevated cTnI concentrations may be detected in some horses 1–14 h after racing. These findings could be of importance when evaluating horses with suspected cardiac disease that recently have performed hard exercise.     

Assessment of a point‐of‐care cardiac troponin I test to differentiate cardiac from noncardiac causes of respiratory distress in dogs

Objectives – To (1) determine a reference interval for cardiac troponin I (cTnI) using a point‐of‐care device in normal dogs and compare the results with those published by the manufacturer and (2) determine if cTnI differs among dogs with cardiogenic and noncardiogenic respiratory distress. Design – Prospective observational study. Setting – Emergency and referral veterinary hospital. Animals – Twenty‐six clinically normal dogs and 67 dogs in respiratory distress. Interventions – All dogs underwent whole blood sampling for cTnI concentrations. Measurements and Results – Normal dogs had a median cTnI concentration of 0.03 ng/mL (range 0–0.11 ng/mL). Thirty‐six dogs were diagnosed with noncardiogenic respiratory distress with a median cTnI concentration of 0.14 ng/mL (range 0.01–4.31 ng/mL). Thirty‐one dogs were diagnosed with cardiogenic respiratory distress with a median cTnI concentration of 1.74 ng/mL (range 0.05–17.1 ng/mL). A significant difference between cTnI concentrations in normal dogs and dogs with noncardiogenic respiratory distress was not detected. Significant differences in cTnI concentrations were found between normals versus cardiogenic and cardiogenic versus noncardiogenic respiratory distress groups. Significant differences in cTnI concentrations were identified in >10 when compared with the <5 and the 5–10 years of age groups. Receiver operating curve analysis identified cTnI concentrations >1.5 ng/mL as the optimal “cut‐off point” having a sensitivity of 78% and specificity of 51.5%. The area under the receiver operating curve was 0.72. Overall test accuracy was 65%. Conclusions – cTnI concentrations were significantly increased in dogs with cardiogenic respiratory distress versus dogs with noncardiogenic respiratory distress and normal dogs. A significant difference between normal dogs and dogs with noncardiogenic causes of respiratory distress was detected. Although highly sensitive when cTnI concentrations exceed 1.5 ng/mL, the test has low specificity. Assessment of cTnI by the methodology used cannot be recommended as the sole diagnostic modality for evaluating the cause of respiratory distress in dogs.     

Ability of pulse wave transit time to detect changes in stroke volume and to estimate cardiac output compared to thermodilution technique in isoflurane-anaesthetised dogs

Objective

To evaluate the ability of pulse wave transit time (PWTT) to detect changes in stroke volume (SV) and to estimate cardiac output (CO) compared with the thermodilution technique in isoflurane-anaesthetized dogs.

Measurement of respiratory system compliance and respiratory system resistance in healthy dogs undergoing general anaesthesia for elective orthopaedic procedures

Objective The aim of this study was to investigate normal values for the dynamic compliance of the respiratory system (Crs) and respiratory system resistance (Rrs) in mechanically ventilated anaesthetized dogs.Study design Prospective clinical study.Animals Forty healthy dogs undergoing elective orthopaedic surgery. Body weight was (mean ± SD) 26.8 ± 10.7 kg (range: 1.9–45.0 kg), age 4.7 ± 2.9 years (range: 0.1–10.6 years).Methods Dogs were premedicated with acepromazine and methadone administered intramuscularly and anaesthesia induced with propofol intravenously. After endotracheal intubation the dog's lungs were connected to an appropriate breathing system depending on body weight and isoflurane in oxygen administered for maintenance of anaesthesia. The lungs were ventilated mechanically with variables set to maintain normocapnia (end‐tidal carbon dioxide concentration 4.7–6.0 kPa). Peak inspiratory pressure, Crs, Rrs, tidal volume, respiratory rate and positive end‐expiratory pressure were recorded at 5, 30, 60, 90 and 120 minutes after start of mechanical ventilation. Cardiovascular variables were recorded at time of collection of respiratory data.Results General additive modeling revealed the following relationships: Crs = [0.895 × body weight (kg)] + 8.845 and Rrs = [?0.0966 × body weight (kg)] + 6.965. Body weight and endotracheal tube diameter were associated with Crs (p <0.001 and p =0.002 respectively) and Rrs (p = 0.017 and p =0.002 respectively), body weight being linearly related to Crs and inversely to Rrs.Conclusion and clinical relevance Body weight was linearly related to Crs while Rrs has an inverse linear relationship with body weight in mechanically ventilated dogs. The derived values of Crs and Rrs may be used for monitoring of lung function and ventilation in healthy dogs under anaesthesia.     

Serum concentrations of cardiac troponin I and cardiac troponin T in dogs with class IV congestive heart failure due to mitral valve disease

Objective: The objective of this study was to evaluate the incidence of circulating detectable serum levels of cardiac troponin I (CTnI) and circulating detectable serum levels of cardiac troponin T (CTnT) in dogs with class IV congestive heart failure (CHF) due to mitral valve disease (MVD) at admission. An additional study aim was to determine if detectable troponin levels correlated with the magnitude of several clinical parameters. Design: Prospective clinical investigation. Setting: Small animal emergency and critical care referral hospital. Interventions: Blood was collected before emergency treatment from 15 dogs presenting in class IV CHF due to MVD. Measurements: Serum concentrations of CTnI, CTnT at presentation. Main results: Six dogs (40%) had a detectable CTnI (median 0.24, range 0.12–0.31 ng/mL), and the remainder were less than 0.1 ng/mL and deemed non‐detectable. The one dog (7%) that had a detectable CTnT (0.02 ng/mL) also had a detectable CTnI (0.23 ng/mL). There was no statistical difference in survival to discharge between dogs with non‐detectable troponin levels and those with detectable troponin levels; however, dogs with detectable troponin levels had shorter overall survival times. Dogs with a detectable level of CTnI had a median survival of 67.5 days (range 1–390 days), and dogs with a non‐detectable level of CTnI had a median survival time of 390 days (range 20–912 days) (P=0.02). Conclusion: This study suggests that CTnI can be detected at admission in the blood of 40% of dogs with class IV CHF due to MVD. Dogs with non‐detectable levels of cardiac troponins had a significantly longer overall survival time. The encouraging results of this small pilot study warrant further investigation.     

Safety evaluation of combination carboplatin and toceranib phosphate (Palladia) in tumour‐bearing dogs: A phase I dose finding study

Combining conventional cytotoxic maximum tolerated dose (MTD) chemotherapy with low‐dose metronomic and/or anti‐angiogenic agents is a exciting area of oncologic research. The objective of this study was to establish the MTD, safety and adverse event (AE) profile of 1 such drug combination. This prospective phase I dose‐finding clinical trial assumed an open‐label 3 + 3 cohort design. Client‐owned dogs with 1 or more cytologically and/or histologically confirmed and macroscopically measurable, naive or recurrent, malignant tumours, were enrolled. No preference for tumour histology, grade or stage was expressed. Toceranib was administered at a dose of 2.75 mg kg^?1 by mouth (PO) every other day (EOD), and carboplatin administered intravenously (IV) every 21 days at a starting dose of 200 mg m^?2. A total of 25% dose escalation was proposed for carboplatin, to a maximum of 300 mg m^?2. AEs were graded according to the Veterinary Cooperative Oncology Group's common terminology criteria for AEs (VCOG‐CTCAE). Grade 3 haematologic or gastrointestinal AEs were nominated dose‐limiting. Response to therapy was evaluated according to the VCOG's revised RECIST criteria. Eleven dogs were enrolled. Tumour histologies included sinonasal carcinoma, osteosarcoma, thyroid carcinoma, melanoma and apocrine gland anal sac adenocarcinoma. MTDs of carboplatin and toceranib were identified as 200 mg m^?2 IV every 21 days and approximately 2.75 mg kg^?1 PO EOD, respectively. The dose‐limiting toxicity was neutropenia. Two dogs experienced a partial response, and 6 maintained stable disease. Combination carboplatin and toceranib chemotherapy was well‐tolerated. Clinical benefit was observed in most cases. This protocol warrants further investigation in phase II/III trials.     

A comparison in dogs of medetomidine,with or without MK‐467, and the combination acepromazine‐butorphanol as premedication prior to anaesthesia induced by propofol and maintained with isoflurane

ObjectiveTo compare the haemodynamic effects of three premedicant regimens during propofol-induced isoflurane anaesthesia.Study designProspective, randomized cross-over study.AnimalsEight healthy purpose-bred beagles aged 4 years and weighing mean 13.6 ± SD 1.9 kg.MethodsThe dogs were instrumented whilst under isoflurane anaesthesia prior to each experiment, then allowed to recover for 60 minutes. Each dog was treated with three different premedications given intravenously (IV): medetomidine 10 μg kg^?1 (MED), medetomidine 10 μg kg^?1 with MK-467 250 μg kg^?1 (MMK), or acepromazine 0.01 mg kg^?1 with butorphanol 0.3 mg kg^?1 (AB). Anaesthesia was induced 20 minutes later with propofol and maintained with isoflurane in oxygen for 60 minutes. Heart rate (HR), cardiac output, arterial blood pressures (ABP), central venous pressure (CVP), respiratory rate, inspired oxygen fraction, rectal temperature (RT) and bispectral index (BIS) were measured and arterial and venous blood gases analyzed. Cardiac index (CI), systemic vascular resistance index (SVRI), oxygen delivery index (DO₂I), systemic oxygen consumption index (VO₂I) and oxygen extraction (EO₂) were calculated. Times to extubation, righting, sternal recumbency and walking were recorded. The differences between treatment groups were evaluated with repeated measures analysis of covariance.ResultsHR, CI, DO₂I and BIS were significantly lower with MED than with MMK. ABP, CVP, SVRI, EO₂, RT and arterial lactate were significantly higher with MED than with MMK and AB. HR and ABP were significantly higher with MMK than with AB. However, CVP, CI, SVRI, DO₂I, VO₂I, EO₂, T, BIS and blood lactate did not differ significantly between MMK and AB. The times to extubation, righting, sternal recumbency and walking were significantly shorter with MMK than with MED and AB.Conclusions and clinical relevanceMK-467 attenuates certain cardiovascular effects of medetomidine in dogs anaesthetized with isoflurane. The cardiovascular effects of MMK are very similar to those of AB.     

Clinicopathologic features and outcome predictors of Leptospira interrogans Australis serogroup infection in dogs: a retrospective study of 20 cases (2001-2004)

BACKGROUND AND HYPOTHESIS: We retrospectively evaluated the clinicopathologic findings and outcome predictors in dogs with Leptospira interrogans Australis serogroup infections. ANIMALS AND METHODS: The medical records of 159 dogs that had a leptospiral microscopic agglutination test (MAT) performed between 2001 and 2004 were reviewed. RESULTS: Twenty dogs met serologic criteria for either symptomatic (16 dogs) or asymptomatic (4 dogs) infection caused by Leptospira interrogans Australis serogroup. Seven of 16 symptomatic dogs died or were euthanized and 9/16 recovered. Systemic inflammatory response syndrome (SIRS) was observed in 9/16 dogs. The presence of SIRS did not affect prognosis (P = .357). C-reactive protein (CRP) and haptoglobin (Hpt) concentrations were altered in all symptomatic dogs, but results did not differ significantly between survivors and nonsurvivors (P = .08 and P = .055, respectively). Conversely, the CRP to Hpt ratio (CRP/Hpt) was significantly increased in nonsurvivors. Disseminated intravascular coagulation (DIC) was diagnosed in 7/16 dogs. DIC did not significantly affect outcome (P = .126). Multiple organ involvement was present with renal failure in 16/16, liver damage in 12/16, cardiac damage in 11/16, and muscular damage in 8/16 dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: Among the evaluated clinicopathologic biomarkers, serum albumin, cardiac troponin I, CRP/Hpt, urinary albumin, and urinary total protein to creatinine ratio were found to predict outcome and warrant evaluation in larger prospective studies.