Syncope secondary to transient atrioventricular block in a German shepherd dog with dilated cardiomyopathy and atrial fibrillation

This case report describes transient atrioventricular block as the etiology for syncopal events in a 6-year-old male German shepherd dog with atrial fibrillation and dilated cardiomyopathy. The arrhythmia diagnosis was obtained via Holter monitoring. Medical treatment with a sustained-release preparation of theophylline, as an additive to the standard congestive heart failure treatment (benazepril, furosemide and pimobendan) may have contributed to temporary remission of the syncopal events. However, the congestive heart failure progressed and the dog was euthanized. Veterinarians should be aware of the possibility of transient atrioventricular block causing syncope in dogs with DCM and AF and should be careful in empirically lowering the ventricular response rate if these dogs present with syncopal episodes.     

Finding cardiovascular disease genes in the dog

Recent advances in canine genomics are changing the landscape of veterinary biology, and by default, veterinary medicine. No longer are clinicians locked into traditional methods of diagnoses and therapy. Rather, major advances in canine genetics and genomics from the past five years are now changing the way the veterinarian of the 21st century practices medicine. First, the availability of a dense genome map gives canine genetics a much-needed foothold in comparative medicine, allowing advances made in human and mouse genetics to be applied to companion animals. Second, the recently released 7.5× whole genome sequence of the dog is facilitating the identification of hereditary disease genes. Finally, development of genetic tools for rapid screening of families and populations at risk for inherited disease means that the cost of identifying and testing for disease loci will significantly decrease in coming years. Out of these advances will come major changes in companion animal diagnostics and therapy. Clinicians will be able to offer their clients genetic testing and counseling for a myriad of disorders. In this review we summarize recent findings in canine genomics and discuss their application to the study of canine cardiac health.     

Evaluation of cardiac performance of the dog after induction of portal hypertension and gastric ischemia

Objective: To determine changes in hemodynamic and cardiac energetic parameters in dogs after induction of portal hypertension and gastric ischemia. These blood flow alterations are similar to changes seen in splanchnic blood flow in dogs with gastric dilatation volvulus syndrome (GDV). Design: Original experimental study. Setting: Veterinary teaching hospital. Animals: Seven purpose‐bred, intact male dogs. Interventions: Standard midline laparotomy and median sternotomy were performed under general anesthesia. Dogs were instrumented to obtain arterial blood pressure, aortic flow, cardiac chamber pressures, central venous pressure, portal flow, and portal pressure. Colored microsphere technology was used for the determination of myocardial blood flow. Measurements and samples were obtained at baseline, following induction of portal hypertension, and after induction of portal hypertension and gastric ischemia. Measurements and main results: Left ventricular myocardial blood flow was increased from 81.8±20.1 mL/100 g/min at baseline to 127.7±57.2 mL/100 g/min (P=0.02) after induction of portal hypertension and gastric ischemia. Myocardial oxygen consumption increased from 142.2±27.4 J/min/100 g at baseline to 219.1±33.4 J/min/100 g (P=0.003) after induction of portal hypertension and gastric ischemia, but cardiac external work remained unchanged (13.67±6.2 to 13.27±9.6 J/min; P=0.78; power=0.79). Cardiac efficiency decreased from 11.6±6.1% at baseline to 7.6±5.1% (P=0.017) after induction of portal hypertension and gastric ischemia. Conclusions: Transfer of energy within the myocardium was less efficient after induction of portal hypertension and ischemia of the stomach wall. On the basis of these results, alterations in cardiac function associated with GDV may result from deterioration of cardiac efficiency.     

Amanita muscaria toxicosis in two dogs

Objective: To report the manifestations, history, and pathophysiologic basis of disease in 2 dogs with Amanita muscaria toxicosis. Case summaries: Two dogs were evaluated for an acute onset of gastroenteritis and seizures. A. muscaria toxicosis was suspected in each dog after confirmation of environmental exposure and visualization of ingested mushrooms in vomitus. The diagnosis was confirmed following identification of toxic Amanita metabolites in the urine and serum of each dog. Administration of supportive and symptomatic therapies resulted in the complete recovery of each animal. Unique information provided: Ingestion of the mushroom, A. muscaria, by dogs can result in acute gastrointestinal distress that precedes a potentially life‐threatening central neurologic syndrome characterized by seizures, tremors, and somnolence. Central nervous system dysfunction results primarily from the actions of ibotenic acid and its decarboxylation product, muscimol, which are analogues of the neurotransmitters glutamate and γ‐aminobutyric acid (GABA), respectively. Identification of these toxins in the urine and serum of affected dogs using high‐performance liquid chromatography (HPLC) provides a definitive diagnosis.     

Detomidine-Butorphanol-Propofol for Carotid Artery Translocation and Castration or Ovariectomy in Goats

Objective—To determine the safety and efficacy of propofol, after detomidine-butorphanol premedication, for induction and anesthetic maintenance for carotid artery translocation and castration or ovariectomy in goats. Study Design—Case series. Animals—Nine 4-month-old Spanish goats (17.1 ± 2.6 kg) were used to evaluate propofol anesthesia for carotid artery translocation and castration or ovariectomy. Methods—Goats were premedicated with detomidine (10 μg/kg intramuscularly [IM]) and butorphanol (0.1 mg/kg IM) and induced with an initial bolus of propofol (3 to 4 mg/kg intravenously [IV]). If necessary for intubation, additional propofol was given in 5-mg (IV) increments. Propofol infusion (0.3 mg/kg/min IV) was used to maintain anesthesia, and oxygen was insufflated (5 L/min). The infusion rate was adjusted to maintain an acceptable anesthetic plane as determined by movement, muscle relaxation, ocular signs, response to surgery, and cardiopulmonary responses. Systolic (SAP), mean (MAP) and diastolic (DAP) arterial pressures, heart rate (HR), ECG, respiratory rate (RR), Spo₂, and rectal temperature (T) were recorded every 5 minutes postinduction; arterial blood gas samples were collected every 15 minutes. Normally distributed data are represented as mean ± SD; other data are medians (range). Results—Propofol (4.3 ± 0.9 mg/kg IV) produced smooth, rapid (15.2 ± 6 sec) sternal recumbency. Propofol infusion (0.52 ± 0.11 mg/kg/min IV) maintained anesthesia. Mean anesthesia time was 83 ± 15 minutes. Muscle relaxation was good; eye signs indicated surgical anesthesia; two goats moved before surgery began; one goat moved twice during laparotomy. Means are reported over the course of the data collection period. Means during the anesthesia for pH_a (arterial PH), P_aco₂, P_ao₂, HCO₃, and BE (base excess) ranged from 7.233 ± 0.067 to 7.319 ± 0.026, 54.1 ± 4.6 to 65.3 ± 12.0 mm Hg, 133.1 ± 45.4 to 183.8 ± 75.1 mm Hg, 26.9 ± 2.6 to 28.2 ± 2.1 mEq/L, and -0.8 ± 2.9 to 1.4 ± 2.2 mEq/L. Means over time for MAP were 53 ± 12 to 85 ± 21 mm Hg. Mean HR varied over time from 81 ± 6 to 91 ± 11 beats/minute; mean RR, from 9 ± 8 to 15 ± 5 breaths/minute; S_po₂, from 97 ± 3% to 98 ± 3%; mean T, from 36.0 ± 0.6±C to 39.1 ± 0.7±C. Over time, S_po₂ and S_ao₂ did not change significantly; HR, RR, T, and P_aco₂ decreased significantly; SAP, DAP, MAP, pH_a, P_ao₂, and BE increased significantly. HCO₃ concentrations increased significantly, peaking at 45 minutes. Recoveries were smooth and rapid; the time from the end of propofol infusion to extubation was 7.3 ± 3 minutes, to sternal was 9.2 ± 5 minutes, and to standing was 17.7 ± 4 minutes. Median number of attempts to stand was two (range of one to four). Postoperative pain was mild to moderate. Conclusions—Detomidine-butorphanol-propofol provided good anesthesia for carotid artery translocation and neutering in goats. Clinical Relevance—Detomidine-butorphanol-propofol anesthesia with oxygen insufflation may be safely used for surgical intervention in healthy goats.     

Neuromuscular Effects of Doxacurium Chloride in Isoflurane-Anesthetized Dogs

Objective—To determine the neuromuscular effects of doxacurium chloride and to construct a dose-response curve for the drug in isoflurane-anesthetized dogs. Design—Randomized, controlled trial. Animals—Six healthy, adult, mixed-breed dogs (five female, one male) weighing 24.8 ° 2.8 kg. Methods—Anesthesia was induced with isoflurane in oxygen and maintained with 1.9% to 2.3% end-tidal isoflurane concentration. Paco₂ was maintained between 35 and 45 mm Hg with mechanical ventilation. Mechanomyography was used to quantitate the evoked twitch response of the paw after supramaximal train-of-four stimulation of the superficial peroneal nerve. After baseline values were recorded, the dogs received one of three doses of doxacurium (2.0, 3.5, 4.5 μg/kg of body weight) or a saline placebo intravenously in random order. All dogs received all treatments with at least 7 days between studies. After drug administration, the degree of maximal first twitch depression compared with baseline (T,%) was recorded. Dose-response relations of doxacurium were plotted in log dose-probit format and analyzed by linear regression to determine effective dose (ED₅₀ and ED₉₀) values for doxacurium. Results—The median log dose-probit response curve showed good data correlation (r= .999) with estimates of the ED₅₀ (2.1 μg/kg) and ED₉₀ (3.5 μg/kg) for doxacurium in isoflurane-anesthetized dogs. Mean ± SD values for T₁% (first twitch tension compared with baseline) at maximal depression after drug administration, onset (time from drug administration to maximal depression of T₁%), duration (time from maximal depression of T₁% to 25% recovery of T₁%), and recovery (time from 25% to 75% recovery of T₁%) times were 92%± 4%, 40 ± 5 minutes, 108 ± 31 minutes, and 42 ± 11 minutes for dogs treated with 3.5 μg/kg of doxacurium and 94%± 7%, 41 ± 8 minutes, 111 ± 33 minutes, and 37 ± 10 minutes for dogs treated with 4.5 μg/kg of doxacurium. Conclusion and Clinical Relevance—We conclude that doxacurium is a long-acting neuromuscular blocking agent with a slow onset of action. Doxacurium can be used to provide muscle relaxation for long surgical procedures in isoflurane-anesthetized dogs. Interpatient variability, particularly of duration of drug action, may exist in the neuromuscular response to the administration of doxacurium in dogs.