QUANTITATIVE ASSESSMENT OF SURGICALLY INDUCED MITRAL REGURGITATION USING RADIONUCLIDE VENTRICULOGRAPHY AND FIRST PASS RADIONUCLIDE ANGIOGRAPHY

Radionuclide ventriculography has been used in humans to evaluate valvular incompetency. The stroke volume ratio, derived from the radionuclide ventriculogram, is used to quantify the severity of mitral regurgitation (MR). Previous studies conducted in humans have shown that left to right stroke volume ratio increases as the severity of MR increases. In this study, we evaluated radionuclide ventriculography as a noninvasive method to detect MR in dogs with surgically created mitral insufficiency. Six male and three female adult, conditioned mongrel dogs were used. Scintigraphic studies were performed prior to and 4 weeks after surgically created MR. Because of the overlap of the left and right ventricles when viewed from a left lateral position, we combined data from a first-pass radionuclide angiocardiogram with the radionuclide ventriculogram to obtain a corrected stroke volume ratio. Blood flow transit parameters were also derived from the first-pass radionuclide angiocardiogram. Standard left ventricular functional indices were also measured from the radionuclide ventriculogram. On the left lateral view of the heart, 25 to 30% of the right ventricular volume overlaps the left ventricle. After correcting for the overlap, the stroke volume ratio of normal dogs was 1.17±0.178 (mean±SD), which increased to 2.06±0.41 (mean±SD) (p<.001) 4 weeks after creation of MR. The was no significant change in left ventricular ejection fraction or peak rate of ejection following MR. The transit times of blood through the left ventricle were measured from the first-pass radionuclide angiocardiogram and were expressed as half-time clearance, peak clearance rate, and time to peak clearance rate. The baseline half-time clearance was 2.07±0.71 s (mean±SD), which increased to 6.70±4.89 s (mean±SD) (p=.02) after creation of MR. The baseline peak clearance rate was 49.75±8.96 cts/s (mean±SD), which decreased to 23.12±6.84 cts/s (mean±SD) (p<.001) after creation of MR. Stroke volume ratios significantly increased following creation of MR. Blood flow transit through the left ventricle slowed following creation of MR. The variability of these parameters were small in the baseline studies, suggesting these techniques may be clinically useful to gauge the severity of MR in dogs.     

Influence of Cholinergic Blockade on the Development of Epinephrine-Induced Ventricular Arrhythmias in Halothane- and Isoflurane-Anesthetized Dogs

The arrhythmogenic effects of anesthetic drugs are assessed using the arrhythmogenic dose of epinephrine (ADE) model. The purpose of this study was to determine the influence of cholinergic blockade (CB) produced by glycopyrrolate (G) on ADE in 1.5 minimum alveolar concentration (MAC) halothane (H)- and isoflurane (I)-anesthetized dogs. Eight dogs (weighing between 12.5 and 21.5 kg) were randomly assigned to four treatment groups (H, HG, I, and IG) and each treatment was replicated three times. Anesthesia was induced and maintained with H (1.31%, end-tidal [ET]) or I (1.95%, ET) in oxygen. Ventilation was controlled (carbon dioxide [PCO₂] 35 to 40 mmHg, ET). G was administered 10 minutes before ADE determination at a dose of 22 μg/kg (11 μg/kg, intravenous [IV] and 11 μg/kg, intramuscular [IM]). The ADE was determined by IV infusion of epinephrine at sequentially increasing rates of 1.0, 2.5, and 5.0 μg/kg/min; and defined as the total dose of epinephrine producing at least four ectopic ventricular contractions (EVCs) within 15 seconds during a 3-minute infusion and up to 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Data were analyzed using a randomized complete block analysis of variance. When significant (P < .05) F values were found a least significant difference test was used to compare group means. Values are reported as means ± standard error. The ADE (μg/kg) for H, HG, I, and IG were 1.53 ± 0.08, 3.37 ± 0.46, 1.61 ± 0.21, and > 15.00, respectively. Heart rates (HRs) (beats/min) and systolic pressures (mmHg) at the time of arrhythmia formation for H, HG, I, and IG were (60.3 ±4.0 and 142.0 ± 7.6), (213.0 ± 13.1 and 239.2 ± 7.1), (62.9 ± 4.5 and 151.9 ± 6.3), and (226.3 ± 6.1 and 323.5 ± 3.4), respectively. The H and I ADE were not different. The HG ADE was significantly less than the IG ADE. The H and I ADE were significantly less than the HG and IG ADE. We conclude the following from the results of this study of epinephrine infusion in halothane- and isoflurane-anesthetized dogs: (1) two distinct mechanisms are responsible for the development of arrhythmias, (2) CB produced by G significantly increases ADE but is associated with higher rate pressure products (RPP) and myocardial work, and (3) ADE methodology could be improved by determining ADE with and without CB.     

Evaluation of Transmittance and Reflectance Pulse Oximetry in a Canine Model of Hypotension and Desaturation

Ten, anesthetized dogs were instrumented with three pulse oximeter probes; two lingual transmittance probes and one rectal reflective probe. Arterial oxygen desaturation was produced by decreasing the inspired oxygen concentration. Hypotension was produced with an infusion of nitroprusside. Simultaneous pulse oximeter readings (SpO₂) were compared to co-oximeter measured arterial saturation (SaO₂) collected over a range of SaO₂ (50–100%) and mean arterial pressures (40–100mmHg). Each of the monitors and means of evaluating SpO₂ studied provided accurate SpO₂ measurements over a range of mean arterial pressure from 40–100mmHg. All of the monitors tested tended to overestimate the SaO₂ when the arterial saturation was less than 70%.     

SONOGRAPHIC EVALUATION OF THE CRANIAL MEDIASTINUM IN SMALL ANIMALS

Clinical records, radiographs, and sonograms of 17 animals presented for possible cranial mediastinal disease were reviewed. Radiographs were evaluated for accuracy in detection of mediastinal masses. Sonography of the mediastinum was performed using a parasternal approach with the animals in sternal or lateral recumbency. The mediastinum was evaluated for the presence of a mass or other disease. Masses were characterized by echogenicity, size, number, and margination. Mediastinal vessels were studied to determine if there was vascular invasion or compression. A comparison of radiographic and sonographic assessment in cranial mediastinal disease indicates sonography adds valuable information in the diagnosis of mediastinal disease. Results of ultrasound-guided, fine-needle aspirate were documented and found to be advantageous in establishing a diagnosis in mediastinal masses.     

Thrombolytic Therapy in Dogs and Cats

Objective: To review the thrombolytic agents most commonly used in humans, their mechanisms of action, potential uses, adverse effects, and reports of their use in dogs and cats.
Human data synthesis: Thrombolytic agents avaliable in human medicine include streptokinase, urokinase, tissueplasminogen activator (t-PA), single-chain urokinase plasma activator (scu-PA) and anisoylated plasminogen-strep-tokinase activator complex (APSAC). These agents were originally used for the management of proximal deep vein thrombosis and severe pulmonary embolism but more recently, use of these drugs has been extended to include the treatment of acute peripheral arterial disease, cerebrovascular disease (stroke) and acute coronary thrombosis. The most predictable side effect associated with the use of thrombolytic therapy is hemorrhage.
Veterinary data synthesis: Clinical experience with thrombolytic agents in small animals is limited to streptokinase and t-PA. It is possible, that as in humans, canine and feline patients with PTE and right ventricular dysfunction may benefit from thrombolytic therapy but there are no veterinary studies to support this theory to date. Successful use of streptokinase has been documented in a small number of canine patients with systemic thromboembolism. ⁶³ Thrombolytic therapy is relatively efficacious in cats with aortic thromboemboli but is associated with a high mortality rate. ^59,60,64 With regard to use of t-PA in veterinary medicine, the small number of animals treated with varying protocols makes it impossible to provide safe and effective dose recommendations at this time.
Conclusions: Future goals for thrombolytic therapy in veterinary medicine include determination of more specific clinical indications, as well as design of effective protocols that minimize mortality and morbidity.     

Intraperitoneal Circulation and Drainage in the Dog

The patterns of dispersion and drainage of a low viscosity, oil-based contrast medium within the peritoneal cavity were examined in 12 normal dogs. Intraperitoneal injection of contrast medium was cranial or caudal and drainage was by the sump-Penrose or open peritoneal method. Radiographs were made over a 96 hour period, before and after peritoneal drainage was established. Each dog was euthanatized and necropsied. The contrast medium was dispersed throughout the peritoneal cavity 15 to 30 minutes after cranial injection and 1 to 2 hours after caudal injection. Most of the contrast medium drained within 6 hours after open peritoneal drainage and within 24 to 48 hours after sump-Penrose drainage. At necropsy, there was complete encasement of all sump-Penrose drains and partial occlusion of all open peritoneal incisions by omentum adhered to the abdominal wound edges. Peritonitis was not grossly evident, but all dogs showed histologic evidence of an acute inflammatory reaction associated with the drain or wound edge.     

Postanesthetic Pulmonary Edema In an Arab Stallion

A six-year-old arabian stallion was admitted to The Ohio State University Veterinary Hospital for evaluation and repair of a comminuted fracture of the second phalanx. The horse developed impaired arterial oxygenation during surgey and pulmonary edema post-operatively. We postulate that impaired arterial oxygenation resulted from atelectasis of the dependent lung during annesthesia, and the pulmonary edema occurred following re-expansion of the atelectatic of the initiating cause of the edema, removal of excess lung water from the alveoli, and restoration of normal arterial oxygenation. The horse was fully recovered within 12 hours of initiation of clinical signs of respiratory compromise. The horse was fully recovered within 12 hours of initiation of clinical signs of respiratory compromise. This report describes re-expansion pulmonary edema due to reperfusion injury in a horse, treatment of the condition, and a possible explanation of the pathogenesis of this pulmonary pathology.