Surgical palliation of severe tricuspid valve stenosis in a dog by use of Fontan's procedure.

OBJECTIVE: To describe surgical treatment of tricuspid valve stenosis using the Fontan procedure in a young dog. STUDY DESIGN: Case report. SAMPLE POPULATION: One client-owned dog RESULTS: A six month old female Labrador retriever was diagnosed with tricuspid obstruction. The dog had a displaced tricuspid valve and small right ventricle and had progressed to right-sided (backward) cardiac failure. A Fontan procedure (connection of the right atrium to the pulmonary artery with a prosthetic conduit) was performed. Within three days the right atrial pressure had dropped from a preoperative value of 33 mm Hg to 8 mm Hg and the ascites was significantly reduced. The dog died suddenly two months after surgery. Postmortem examination of the heart showed a greatly enlarged right atrium and hypoplastic right ventricle. The tricuspid valve leaflets were fused and displaced ventrally leaving an opening measuring 3x5 mm between the chambers. The conduit was intact with no evidence of leakage or thrombosis. CONCLUSIONS: Palliation of tricuspid stenosis using the Fontan procedure can be performed in dogs. Sudden death may occur and is most likely because of cardiac arrythmias.

Cyanosis and congenital methemoglobinemia in a puppy.

A six-month-old Pomeranian was referred for evaluation of cyanosis. The puppy had been cyanotic since it was acquired at six weeks of age, but otherwise appeared normal. Diagnostics were aimed at the most common causes (i.e., congenital defects in the cardiovascular and respiratory systems) of cyanosis in a juvenile animal. No clinically significant abnormalities were detected on evaluation of thoracic radiographs, echocardiogram, cardiac color-flow Doppler examination, or blood gases. At this point, a dysfunction in hemoglobin was considered as a possibility. Methemoglobinemia due to deficiency of methemoglobin reductase enzyme was diagnosed based on a specific assay.

Experimental evaluation of central venous pressure monitoring in the dog.

The measurement of central venous pressure (CVP) will provide objective information about intravascular blood volume. Limitations exist with direct and indirect methods of measuring CVP; however, the purpose of this study was to determine if such factors as catheter size, patient position, or measurements taken with either a water manometer or a strain-gauge transducer would affect the accuracy of CVP measurements. The study population consisted of six adult, mixed-breed dogs. Catheter sizes evaluated were 16- and 19-gauge. Patient positions evaluated were right and left lateral recumbencies. Right atrial pressures (RAPs) were used as the reference standards for CVP measurements. Measurements of RAP and CVP were obtained with a water manometer and a strain-gauge transducer. No significant differences were observed in measured CVPs for the effects of catheter size and right versus left lateral recumbency. A 2.7-mmHg difference in water manometry was demonstrated when compared to strain-gauge transducer measurements. Also, strain-gauge transducer measurements had less precision compared to water manometer measurements.

Myocardial buffering capacity and high-energy phosphate utilization during hypothermic circulatory arrest and recovery in the newborn lamb in vivo.

UNLABELLED: The purpose of this study was to measure myocardial buffering capacity and adenosine triphosphate utilization rates in the newborn animal in vivo during hypothermic circulatory arrest and recovery. METHODS: These studies were performed with 31P magnetic resonance spectroscopic techniques, which supplied a 12- to 16-second time resolution, to monitor intracellular pH and phosphocreatine and adenosine triphosphate levels. All experiments were performed with a radiofrequency surface coil on the pericardium with the sheep centered inside a 4.7 T magnet. Newborn sheep (n = 5, aged 16 days +/- 2.4 standard error) were supported by cardiopulmonary bypass, cooled to 20 degrees C, and subjected to 20 minutes of circulatory arrest. RESULTS: During early ischemia, phosphocreatine hydrolysis progressed at a linear rate, 1.2 +/- 0.05 mumol/gm per minute, and was accompanied by intracellular alkalinization. Myocardial buffering capacity calculated from delta pH/delta phosphocreatine equals 25 +/- 3 mueq gm-1 delta pH-1, a value similar to that obtained from perfused heart studies. After the initial 4 minutes in ischemia, the decrease in phosphocreatine hydrolysis was accompanied by intracellular acidification, which is likely due to late induction of anaerobic metabolism. CONCLUSIONS: In these studies, early phosphocreatine hydrolysis rate is nearly equivalent to adenosine triphosphate utilization rate. During the early period of ischemia phosphocreatine hydrolysis serves a buffering function and is associated with intracellular alkalinization. These techniques and measurements can be used to compare effects of myocardial preservation techniques on intracellular pH and adenosine triphosphate kinetics.

Atrial septal defect and ventricular septal defect.

In summary, ASD and VSD sometimes do not require surgical intervention and have a good-to-excellent prognosis in animal patients in which surgical intervention is necessary. Animal patients with these diseases often do not show symptoms, but those that do and cannot be adequately managed medically are challenging but rewarding cardiac surgical cases.

The effect of resuscitation technique and pre-arrest state of oxygenation on blood-gas values during cardiopulmonary resuscitation in dogs.

Large mongrel dogs were anesthetized, instrumented, and subjected to electrically induced ventricular fibrillation after breathing either 100% oxygen (O2) or 10% O2 and 90% nitrogen for 10 minutes before arrest. Four minutes after arrest, open chest cardiopulmonary resuscitation (CPR) or intermittent abdominal compression closed chest CPR was initiated and continued for 20 minutes, at which time defibrillation was attempted. Central arterial and mixed venous blood samples were collected serially for the measurement of pH, carbon dioxide partial pressure (PCO2), and O2 partial pressure (PO2), and calculation of bicarbonate concentration and base excess. Mixed venous blood was collected serially for the measurement of lactate concentration. Hemodynamically variable resuscitation techniques and pre-arrest hypoxia or hyperoxia did not significantly influence blood-gas values during CPR. Mixed venous lactate concentrations after 20 minutes of CPR were significantly higher when hypoxia preceded the arrest and when intermittent abdominal compression closed chest CPR was used for resuscitation. Mixed venous PCO2 was significantly higher than arterial PCO2 in all dogs during CPR but was not significantly different before arrest.

Mixed venous oxygen tension as an estimate of cardiac output in anesthetized horses.

The relationship between mixed venous O2 tension and cardiac output was studied in six anesthetized horses breathing 100% O2. Cardiac output, O2 consumption, mean arterial pressure, heart rate, and arterial and venous blood gases were measured after administration of xylazine or dobutamine to horses in lateral, sternal, and dorsal recumbencies. After approximately 3 hours, Escherichia coli endotoxin was administered while horses were in dorsal recumbency, and all measurements were repeated. Relationships between cardiac index (CI) and PVO2, heart rate, mean arterial pressure, jugular PVO2, and PVO2 of blood from a superficial limb vein were evaluated by linear regression analysis. Mean arterial pressure was significantly (P less than 0.05) correlated with CI in horses in all positions and after endotoxin administration. However, data points were poorly grouped. Heart rate and CI were significantly correlated in horses in all positions, but not after endotoxin administration. Correlations between jugular PVO2 and PVO2 of blood from a superficial limb vein were not significant in horses in sternal recumbency, and PVO2 of blood from a superficial limb vein was not significantly correlated with CI in horses in lateral recumbency. There was a significant and tight correlation between PVO2 and CI in horses in all positions and after endotoxin administration.

Technique for measuring the area of canine articular surfaces.

A method for measuring the surface area of canine articular cartilage was developed. Ten pairs of humeri were harvested from fresh canine cadavers. The articular cartilage of each humeral head was covered with liquid rubber latex applied with a brush to the margins of the articular surface. The latex cast was removed from the cartilage after the latex dried. Radial cuts were made in the cast so it could be flattened into a 2-dimensional plane. The surface area of each cast was then measured, using a compensating polar planimeter.

Primary hypertension in a colony of dogs.

A 5-year-old female Siberian husky that was diagnosed as an essential hypertensive was bred several times over a 5-year period, producing a colony of 39 offspring. Thirty of the 39 animals were subjected to biweekly systemic arterial blood pressure determinations with femoral arterial puncture and were placed into two hypertensive and two normotensive groups based on mean blood pressure: Group 1 (mean blood pressure, 128 +/- 12 mm Hg), Group 2 (mean blood pressure, 121 +/- 3 mm Hg), Group 3 (mean blood pressure, 114 +/- 8 mm Hg), and Group 4 (mean blood pressure, 101 +/- 9 mm Hg). Groups 1, 2, and 3 had mean blood pressures significantly higher than that of Group 4 (p less than 0.05). Ten dogs (representatives from Groups 1, 2, and 3) were subjected to more detailed clinical testing including angiography, echocardiography, ophthalmic examination, plasma catecholamine and renin activity measurements, plasma lead and cadmium determinations, cerebrospinal fluid examination, renal profile, and serum chemistry and hematological analysis. Five unrelated normotensive Siberian huskies were compared with colony dogs by using echocardiography. Groups 1 and 2 showed a clear but statistically insignificant upward trend in left ventricular wall thickness indexed against body weights when compared with that in Group 3 and in the unrelated five normal Siberian dogs. Thus, the only specific difference from group to group in the colony at the termination of this study was the difference in mean blood pressure. Based on these data, it is possible and likely that aging will reveal changes secondary to chronic primary hypertension. The pathogenesis of this hereditary disorder remains unknown.

Pulmonary function in dogs with mitral valve regurgitation.

Mitral valve regurgitation was created in 2 groups of dogs. Groups were selected on absence (group 1) or presence (group 2) of clinical signs of congestive left ventricular failure. Group-2 dogs, in which mean left atrial pressures were greater than 30 mm of Hg, had increases in heart rate, pulmonary arterial mean pressure, left atrial diameter, and left ventricular diastolic diameter. These changes were associated with decreased arterial O2 tension, decreased static and dynamic compliance, reduced lung volumes, and increased pulmonary resistance. Group-1 dogs, in which mean left atrial pressure was less than 30 mm of Hg, had moderate changes in hemodynamics, but no changes in pulmonary function, except during exercise when arterial O2 tension decreased.

Canine essential hypertension: probable mode of inheritance.

Essential hypertension (EH) in dogs is a relatively recently reported phenomenon. In this colony the canine disorder follows family lines and has a probable polygenic mode of inheritance, although the specific mode of inheritance has not been defined since an autosomal dominant trait has not clearly been ruled out. Direct intra-arterial femoral punctures are used to monitor blood pressure elevations, which tend to increase with advancing age. As in man, there are dogs with blood pressures intermediate between affected and normal dogs.

Myocardial tissue iron delocalization and evidence for lipid peroxidation after two hours of ischemia.

Ischemic tissue injury has been proposed to be in part due to oxygen-radical-mediated lipid peroxidation. In vitro studies of such reactions show that they are thermodynamically unfavorable unless catalyzed by transitional metals such as iron in low molecular weight species (LMWS iron), ie, the iron-ADP complex. This study tests for iron delocalization into a LMWS pool during myocardial ischemia and for increased tissue malondialdehyde (MDA), a product of lipid peroxidation. Anesthesia was induced in eight dogs (weighing 20 to 30 kg) with ketamine and maintained by ventilation with 1% halothane. The left anterior descending coronary artery was ligated in four animals, and the circumflex coronary artery was ligated in the other four. Two hours after ligation, the animals were sacrificed by a central venous injection of KCl. Tissue samples were immediately taken from the ischemic zone and from the corresponding nonischemic zone. MDA was determined by the thiobarbituric acid assay. LMWS iron was determined on a tissue ultrafiltrate by the o-phenanthroline assay. Statistical data analysis used the matched-pair two-tailed t test. LMWS iron was 18.3 nM/100 mg in ischemic tissue versus 13.1 nM/100 mg in nonischemic tissue (t = 4.14; P less than .01). MDA was 0.91 nM/100 mg in ischemic tissue versus 0.83 nM/100 mg in nonischemic tissue (t = 7.27; P less than .005). We conclude that there is a significant increase in tissue LMWS iron and in MDA after two hours of regional myocardial ischemia. This iron might be the catalyst for maturation of tissue injury during reperfusion as observed by other investigators.(ABSTRACT TRUNCATED AT 250 WORDS)

Streptokinase treatment of cats with experimentally induced aortic thrombosis.

An investigation was initiated to determine the dosage of streptokinase (given IV) that would consistently produce systemic fibrinolysis, as determined by laboratory evaluation, and to determine the relative safety of this drug in the cat. Results indicated that a loading dose of 90,000 IU of streptokinase (given by continuous infusion over 20 to 30 minutes) and a maintenance dosage (IV) of 45,000 IU of streptokinase/hr predictably produced systemic fibrinolysis in the cat. There were no detectable adverse affects seen on physical examination, necropsy, or histopathologic examination. Using the foregoing dosage regimen, investigation was begun to evaluate the use of streptokinase for treatment of feline thromboembolism. Aortic thrombosis was created experimentally in 15 cats. There was no clearly predictable improvement in nonspecific venous angiograms or thermal circulatory indices for the cats given streptokinase, compared with the values for the control cats. After a total of 180 minutes of treatment, the mean weight of remaining clot removed at necropsy from the aortic trifurcation was 7.3 mg in the streptokinase-treated cats, compared with 13.4 mg in the control cats.

Postischemic tissue injury by iron-mediated free radical lipid peroxidation.

Cell damage initiated during ischemia matures during reperfusion. Mechanisms involved during reperfusion include the effects of arachidonic acid and its oxidative products prostaglandins and leukotrienes, reperfusion tissue calcium overloading, and damage to membranes by lipid peroxidation. Lipid peroxidation occurs by oxygen radical mechanisms that require a metal with more than one ionic state (transitional metal) for catalysis. We have shown that cellular iron is delocalized from the large molecules where it is normally stored to smaller chemical species during postischemic reperfusion. Postischemic lipid peroxidation is inhibited by the iron chelator deferoxamine. Intervention in the reperfusion injury of membranes by chelation of transitional metals is a new and promising therapeutic possibility for protection of the heart and brain.

Efficacy of digoxin administration in dogs with idiopathic congestive cardiomyopathy.

Digoxin administration (0.22 mg/m2 of body surface BID) to 10 large-breed dogs with congestive cardiomyopathy increased shortening fraction more than 5.5% in 4 of the dogs. This group of dogs lived longer than the group that did not have a positive inotropic response to digoxin. Heart rate decreased in both groups of dogs. Base-line jugular PVO2 were low in all dogs. Jugular PVO2 decreased significantly in the group that did not respond to digoxin, presumably because of decreased cardiac output. Jugular PVO2 consistently increased in dogs that had a positive inotropic response to digoxin. Base-line shortening fraction, heart rate, and PVO2 did not predict which dogs would respond to digoxin. Serum digoxin concentrations were consistently between 1.5 and 2.5 ng/ml. It was concluded that digoxin administration is not efficacious in all dogs with congestive cardiomyopathy and that the positive inotropic response is not predicted by base-line shortening fraction, heart rate, or jugular PVO2. Dogs that do respond to digoxin usually live longer than those that do not. Jugular PVO2 can be used to separate dogs that do respond from dogs that do not respond to digoxin as long as the base-line PVO2 is low. The negative chronotropic effects of digoxin may be detrimental to dogs that do not have a positive inotropic effect from digoxin.

Screening coagulation tests in the cat: reference values based on direct venipuncture and catheterized samples.

Platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen degradation products, fibrinogen, and modified thrombin time were determined in 46 healthy adult cats. Samples were obtained by direct venipuncture (pet cats, n=20) or through an 18 gauge intravenous jugular catheter (laboratory conditioned cats, n=26). Range, mean, standard error, and 95% confidence interval were tabulated for the 2 samples. A statistically significant difference between the two groups of cats (Student's t test, p <.05) was found for fibrinogen. No statistical difference was detected between the two groups of cats for the other laboratory values.

Myocardial function in small dogs with chronic mitral regurgitation and severe congestive heart failure.

Systolic myocardial function was assessed in 16 dogs with severe congestive heart failure due to chronic mitral valve fibrosis. End-systolic diameters were measured on echocardiograms and end-systolic volume indices were calculated. Thirteen of the 16 dogs (81%) had normal or only mildly abnormal myocardial function. These data suggested that myocardial failure is not a prominent factor contributing to signs of heart failure in dogs with mitral regurgitation. Because of these data, the routine use of digitalis glycosides to increase cardiac contractility is seriously questioned in dogs with heart failure secondary to chronic mitral regurgitation.